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Difference between genetic engineering and synthetic biology
I've recently seen the term synthetic biology being used to describe research involving genetic modification of organisms. What is the difference between synthetic biology and genetic engineering?
Is it just a new term for the same thing, or is it something different? Does one of the two terms encompass the other?

Hi @Green. Welcome to SE.Biology. If you'd like to get the benefits of a fully account (such as e-mail notifications and voting), register here.

@Luke: I actually have an account, but I was kind of embarrassed to ask such a soft question on it.

My understanding is that synthetic biology is genetic engineering 2.0. The difference is in the approach. Whereas genetic engineering projects are usually ad hoc, synthetic biology aims to apply proper engineering principles such as standardisation, modularisation, and reusability. Synthetic biologists create and use libraries of standard parts that are characterised, so they can be easily reused in projects. A part could be a gene, a terminator, a promoter, etc.
Synthetic biology also has greater ambitions. The focus is on creating whole systems/circuits of genetic regulation. This means there is a need for computational modelling and understanding of how biological systems work. In this aspect synthetic biology is a sister of systems biology a bit like synthetic chemistry (engineering) is a sister of chemistry (science).
You could of course argue that it's just a marketing ploy to invent a new name for something that is just the next step in genetic engineering, but the differences in approach are quite large and a new name signifies it.
With regards to synthesised vs. PCRed DNA: It doesn't really matter which you use in synthetic biology. However, cheap synthesis is one of the technologies that enable easier synthetic biology. The idea for the future is that you will be able to synthesise whole plasmids and chromosomes instead of having to "cut and paste" DNA. When that happens physical parts repositories will be obsolete, but they will remain crucial in silico. Cheap synthesis is nice, but doesn't make or brake synthetic biology.

I like this answer best - if you look at the partsregistry.org you can see there is a strong desire to put the components into an engineering framework that is more device like.

It seems to me that the difference is mainly semantic, although the aims of synthetic biology are undoubtedly more ambitious than those of genetic engineering in, say, the 80s and 90s.
The Wikipedia page on genetic engineering has this definition of the difference:

Synthetic biology is an emerging discipline that takes genetic engineering a step further by introducing artificially synthesized genetic material from raw materials into an organism.

I must say that for me this doesn't really stand up to close scrutiny. To give just just one example from my own experience - for a long time now yeast geneticists have used PCR to make DNA for targetted gene disruption. This seems to me to fit the definition in the quote: the primers were made chemically and the PCR product was made in vitro using dNTPs as raw materials. (Admittedly the template DNA would be normally produced in vivo.) But I don't think we ever thought that we were doing synthetic biology.
Perhaps the term synthetic biology was intended to herald a new approach that would be more fundable?
I look forward to reading the responses to this rather cynical answer :)

I don't think they mean synthetic as in 'made in the lab using PCR', as for all genetic engineering PCR will be essential at some point (at least, that is how I interpret it). The term synthetic probably is used to refer to specific sequences of nucleotides that are not naturally formed (i.e. they are de novo, synthetic sequences).

I see what you are getting at, but wouldn't most mutagenesis experiments fit this definition? Conversely, if I was to synthesis a gene for a protein but changing as many codons as possible without affecting the amino acid sequence - what would that be?

Interesting point. 'Silent' mutations (those that do not affect the protein sequence) could still affect regulation of transcription - for instance miRNA binding or alternative splicing (this is very situation dependent of course, but I'm just saying that 'silent' mutations don't necessarily have no effect). With mutagenesis I would say it's genetic engineering, as there is no 'synthetic' element to the DNA modification, other than it is done under experimental conditions... an analogous experiment using a manufactured/custom sequence of DNA inserted into the genome would be 'synthetic' IMO.

... however this is just my interpretation of things! I have not seen a concrete definition, so I may well be mistaken. Or indeed, there may not be a concrete definition, and this is quite subjective (like 'bioinformatics' vs 'computational biology'. People agree there is a distinction, but not on where the line is drawn).

PCR is not synthetic; although it involves biological synthesis, it has to start from a template. Synthesis as in synthetic biology involves artificial gene synthesis, i.e. starting just with a sequence on a computer and ending with biological sequence.

They seem to be practically the same, with the exception of the goals. Genetic Engineering is the direct modification of the genes of an organism which results in capabilities being added or taken away. Synthetic Biology aims to modify the behaviors of an organism or integrate the behaviors of multiple organisms into a singular whole.
As is explained in  Andrianantoandro E, Basu S, Karig DK, Weiss R. 2006. Synthetic biology: new engineering rules for an emerging discipline. Molecular systems biology 2: 2006.0028:

One useful analogy to conceptualize both the goal and methods of synthetic biology is the computer engineering hierarchy (Figure 1). Within the hierarchy, every constituent part is embedded in a more complex system that provides its context. Design of new behavior occurs with the top of the hierarchy in mind but is implemented bottom-up. At the bottom of the hierarchy are DNA, RNA, proteins, and metabolites (including lipids and carbohydrates, amino acids, and nucleotides), analogous to the physical layer of transistors, capacitors, and resistors in computer engineering. The next layer, the device layer, comprises biochemical reactions that regulate the flow of information and manipulate physical processes, equivalent to engineered logic gates that perform computations in a computer. At the module layer, the synthetic biologist uses a diverse library of biological devices to assemble complex pathways that function like integrated circuits. The connection of these modules to each other and their integration into host cells allows the synthetic biologist to extend or modify the behavior of cells in a programmatic fashion.

It's notable that in the paper's abstract the words engineer(ing) appear six times whereas synthetic appears just twice! The claim of the abstract is that synthetic biology is a new branch of engineering. The engineered constructs of synthetic biology will no doubt be achieved by use of DNA-based technologies. I stick by what I said in my answer: there is a difference of scope and ambition, but really there is nothing new; as the technologies have advanced and matured, so the possibilities have expanded.

In genetics engineering we use and manipulate natural genetic elements but in synthetic biology we make new gene elements and network.

I am not a big fan of definitions and terminology in molecular biology, because biology is not physics, and things that we might describe and define change, as does our understanding of them. However, as this question has surfaced again after a number of years, it might be worthwhile giving a more recent example of synthetic biology, rather than just defining it. That way the reader can get an idea of what it is about.
I would say that:

Synthetic biology is a particular type of genetic engineering.

Definitions
A reasonable definition of genetic engineering is given by Encyclopedia Britannica:

The artificial manipulation, modification, and recombination of DNA or
  other nucleic acid molecules in order to modify an organism or
  population of organisms.

So this could include making a single base change to inactivate a gene or introducing and expressing the gene for human insulin in, say, yeast.
The definitions of synthetic biology are more contorted, e.g. that from the Royal Society

Synthetic biology is an emerging area of research that can broadly be
  described as the design and construction of novel artificial
  biological pathways, organisms or devices, or the redesign of existing
  natural biological systems.

Example
So why is the expression of insulin in yeast not considered synthetic biology? Basically because it lacks the complexity of a completely novel system. Consider the following description of an arsenic biosensor designed to test for arsenic in drinking water:

“Chris French at Edinburgh University led a team that turned the E.
  coli bacterium into an arsenic sensor by rewiring two genes. One gene
  senses arsenic and activates genes to pump it out of the cell; the
  other allows the bacteria to digest the sugar lactose, producing
  lactic acid. The rewiring involves putting the gene for digesting
  lactose under the control of the arsenic sensor. When arsenic is
  detected, the lactose-digesting gene switches on. The lactic acid it
  produces makes the water more acidic, which can be detected using a
  cheap pH indicator: if the reading is blue, the water is safe; yellow
  means it is dangerous.”

So they have engineered a completely new system with two different genes, which have been modified and their regulation co-ordinated (“rewired” in the article) in an original manner. And there is a tendency to embody some of the complexity into modules that can be reused by others allowing even more complex and sophisticated systems to be constructed.
You could say that the difference from insulin expression in yeast is only a matter of degree, but here the devil is really in the detail.


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Do antisense transcripts have different names than their sense strand transcripts?
I want to find which genes in the human genome can potentially be complementary to a transcript that could act as antisense transcript inhibtion? Are cis-NATs (naturally occuring anti-sense transcripts) considered different transcripts and named differently or do they have the same name as the sense transcript?

If the anti-sense transcript is correctly annotated and in the databases (a very very big if), then it will have a different name. For example, the mouse Msx1 anti-sense transcript has the RefSeq accession NR_027920 while the sense transcript of the same gene is NM_010835.
In general, each transcript that is transcribed from a given locus has a different accession. The same is true for alternatively spliced transcripts. If a given gene has 4 AS transcripts, each of these transcripts will have a different, unique accession. The human insulin receptor gene, for example, has two protein coding transcripts, each with its own accession: NM_000208 and NM_001079817.
You may be interested in a recent analysis of cis-NATs in 10 species[1] and also in NATsDB: Natural Antisense Transcripts DataBase[2].

Osato N, Suzuki Y, Ikeo K, Gojobori T. 2007. Transcriptional Interferences in cis Natural Antisense Transcripts of Humans and Mice. Genetics, 176(2): 1299-1306, doi:10.1534/genetics.106.069484.
Li JT, Zhang Y, Kong L, Liu QR, Wei L. 2008. Trans-natural antisense transcripts including noncoding RNAs in 10 species: implications for expression regulation. Nucleic Acids Research, 36(15):4833-44, doi:10.1093/nar/gkn470.

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What are the olfactory chemicals in whiteboard/permanent markers and what do they bind to in the nose, lungs, and brain?
What are the olfactory chemicals in whiteboard/permanent markers and what do they bind to in the nose, lungs, and brain?

here's another paper that might shed light on the second part of your question... http://www.ploscompbiol.org/article/info%3Adoi%2F10.1371%2Fjournal.pcbi.1002224

personally i find ethanol and its closest homologs smell 'sweet'

That make some sense just looking at the mocules. They both bind to the olfactories in a similar way. using the H-OH side.

The smell of dry erase markers come from the chemicals ethanol, butanol and isopropyl alcohol. Like all chemicals inhaled through the nose, they bind to the Receptor neurons in the located in the back of the nose. The neurons interpret the chemicals using a 'lock-and-key' model but the specific way its coded and perceived in humans is still being researched and the process is not completely understood.

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When are population dynamics models useful?
When are population dynamics models useful? There seems to have been a lot of research about it, but how does it help? If I need data about how a population will evolve under what conditions, I need it because I need data for a decision (such as "can we kill 50% of population X without doing too much damage?"), right? But for that, the model needs to be aware of what causes what. And for that, I have to do experiments, right? Like "let's kill a significant amount of population X and see what happens in the next ten years". I really don't get it.

Leonardo's already given you an excellent answer, but I thought I'd add my perspective. I'm a mathematical epidemiologist, so I'd at least like to believe these types of models are useful.
For me, there are a number of things population dynamics models are especially useful for:

Highlighting data requirements. Yes, models need data, as you've mentioned. But they don't need all their data to come from one source, one study, or even one field. Models are also profoundly useful for showing where we don't have the data we need to fully understand a system. "To make a model where we understand A, we need the values for X, Y, and Z. X is well studied, but Y and Z aren't - though it turns out when we look over the entire parameter space for Z, nothing really changes in our answer. But guys? We could really use a study on Y."
Eliminating guesswork. Models aren't perfect encapsulations of reality - there will always be some simplifying assumptions, etc. But it's better than "going with your gut" - especially for complex problems.
Impossible studies. A ton of what mathematical epidemiology looks at it is areas where studies are either impossible, logistically difficult, or unethical. It would be very hard indeed to only be able to study pandemic response plans, or vaccination strategy only when we had an actual outbreak, or while a new vaccine is being rolled out.
Highlighting potentially new directions. If you're considering an intervention, but no matter how effective you make it in your model it doesn't move the system much, it might not be worthwhile. Models can also highlight threshold effects - like the critical % of the population you'd need to vaccinate to achieve herd immunity.

Wow, that's a really good answer, too! Thank you. :)

Two previous answers listed many applications of population dynamics models. I want to add that they are also important for conservation of endangered species. For example classical stage-class model (Crouse et al 1987, free copy) indicate that the most effective way to protect sea turtles is reducing mortality of large juveniles.
Moreover, you don't have to perform such drastic experiments as killing 50% of  a population to estimate your model parameters. Information about number of offspring, breeding success, natural mortality, etc can usually be gain without serious perturbation of wild populations. The number of individuals in every natural population fluctuates because of random reasons, so it is possible (but sometimes needs more field work) to calculate, (possibly nonlinear) regression between density of population and some demographic indicators and then extrapolate it to non-examined densities. For some small, short-living species it is sometimes possible to measure that correlations in laboratory or semi-wild conditions. For some long-living species, especially if they are sedentary, like trees, it may be better to compare specimens living in different distance from its neighborhoods. For poorly-known species it is possible to take missing information from related or similar species.

I'll throw one more application into the pot. Population dynamics also forms the foundations of population genetics, population ecology, and more recently plays an important role in frameworks such as evolutionary game theory and eco-evolutionary dynamics.
Here the models are also used as a type of theoretical exercise or thought experiment (as a previous answer suggests). In the development of evolutionary theory we simply cannot observe the process over the timescales we require to test the hypotheses we make. Thus, the development of population models allows us to explore 'possible worlds', as Robert May once put it, to see what kinds of adaptations or population structures we would expect to see, given the assumptions we put in.
We are also seeing an increasing number of population models and dynamical models used in conjunction with experiments on microbes in the field of experimental evolution. Here we can observe evolution in real time, and many of the assumptions about well-mixedness and large population sizes that are often made in modelling populations are actually fairly accurate.


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Evolutionary origin and exogenous cues of ~28 day infradian rhythm?
The most obvious example of an approximately monthly biological cycle is the human menstrual cycle. My questions are the following:

Is it known when and where this cycle or one like it arose?
What exogenous cue(s) (if any) is/are this cycle based on? The moon's
orbit around the earth is seemingly obvious however the only cue that
I can think of that would be easily sensed by organisms is variance
in night-time illumination, which seems like a very weak phenomenon
when compared to day/night and seasonal cycles. King and neap tides may be a suitable cue however they have a half-monthly modulation.
The moon has been steadily retreating from the earth over the course
of its history, which means that months have been slowly getting
longer. Is there any fossil (e.g. biogeochemical) evidence of
organisms with biological cycles in synchrony with a 'short month'?

I don't know whether the length of the Moon's orbit is such a good explanation: the menstrual/estral cycle varies a lot amongst species. For instance, mice and rats have a 4/6 days estral cycle, chimpanzees have a 37 days menstrual cycle. Also, many animals go in anestrus (they don't cycle during certain periods of the year).

@nico - Ah, that shows what I know about estrus: I was under the impression that the estral cycle was a single seasonally-modulated cycle rather than a 'cycle within a cycle'. Also didn't know that the chimpanzee menstrual cycle was different. I suspected the periodicity of coral spawning might be an example of an evolutionarily early 28-day clock but wiki seems to suggest that that's a case of an exogenous trigger rather than entrainment.

the difference between estrous cycle and menstrual cycle is essentially that in the estrous cycle there is reabsorption of the endometrium if the animal is not fertilized. The wikipedia article explains it quite well.

A double-blind, prospective study during the fall of 1979 investigated
  the association between the menstrual cycles of 305 Brooklyn College
  undergraduates and their associates and the lunar cycles.
.... Approximately 1/3 of the subjects had lunar period cycles, i.e.
  a mean cycle length of 29.5 ± 1 day. Almost 2/3 of the subjects
  started their October cycle in the light 1/2 of the lunar cycle,
  significantly more than would be expected by random distribution. The
  author concludes that there is a lunar influence on ovulation.

(Menstrual and Lunar Cycles, Friedmann E., American Journal of Obstetrics and Gynecology, 1981)
Another source supports this conclusion, finding that "a large proportion of menstruations occurred around the new moon."
Somewhat related, this study found that light exposure shortened menstruation cycles.
In summary, there seems to be a good amount of data suggesting that lunar cycles do in fact calibrate the length of human menstrual cycles to some degree.

There seems to be some data suggesting that the two are correlated. As to causation I think we're not even close to prove that.

@nico Well, if they are correlated but lunar cycles do not affect menstrual cycles, then there are two other possibilities. Either menstrual cycles affect lunar cycles, or a confounding factor affects both lunar cycles and menstrual cycles. Neither of these seem very likely. Additionally, we know that light exposure seems to have some effect on cycle length.

then why would it only work for humans and not for other primates?

@MatthewPiziak: correct me if I'm wrong, but isn't there a third possibility as well - that the lunar cycle affects something which is the causation of the human menstrual cycle.
nico - I have no idea about the cycles of other relative close ancestors to us (ie primates), but do you know if they deviate substantially from the human cycle?


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What are limiting factors for intron length?
For predicting genes from a sequenced genome, you need to set a maximum intron length. How long can introns get in animals? Is there some limit?

I don't know about the maximum length, but I suppose that for the minimal size, the mechanical properties of the DNA are the limiting factors. Under a certain size, DNA is simply too stiff to form the loops required during splicing.

I think the above values (500-750 kb) are wrong.  http://www.bioinfo.de/isb/2004040032/ shows that most introns are less than about 10 kb (and personal experience in Drosophila confirms that - I've rarely seen an intron bigger than about 5 kb).  There are some very large ones, but since it's nearly impossible to detect the splicing reaction, particularly if they're very large, it's not clear whether they are spliced as one BIG intron or are instead recursively spliced (in little steps, as in http://www.genetics.org/content/170/2/661.full.pdf+html).  I think its safe to say that we don't know how long the biggest introns can be.

If you examine the human genome ~99% of the introns are under 500 kb. I would assume that a limit between 250 kb - 500 kb is reasonable for gene prediction.  You may incorrectly predict the proper structure of a small number of genes that have these very large introns but this should be a small number.  Furthermore, most popular sequence aligners tend to set an intron length limit between 500 kb and 750 kb.
Just keep in mind that you may increase the number of false positive introns you detect if you set this limit to high.  Therefore, it may be worthwhile to try a few settings and evaluate the results.
EDIT:
My guess is that larger introns are constrained in mammals for two reasons

They are more difficult for the spliceosome to excise properly.  The spliceosome may have reduced assembly at the proper 5' / 3' splice sites and the branch point site.  There is also a higher chance that there will be cryptic / decoy splice sites witihin the intron.
They increase the time it takes to transcribe the gene


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Factor causing Methicilin-resistance in MRSA?
I think the main reason is the natural selection that is causing methicillin-resistance.
However, I am not completely sure what this means practically.
Here, the original question:
MRSA was isolated in the throat secretion of patient hospitalized with bronchitis. Which of the following
statements best characterizes this microorganism?

a. its MIC is increased to methicillin, but not to penicillin
b. methicillin-resistance is associated with production of β-lactamases
c. Methicillin-resistance is caused by changes in configuration (mutation) of PBP

What is the right answer?

Thanks for editing and adding the full question.  I will update my answer.  Just to clarify what you meant, in your answer you say that you think the answer is B but then describe C?  I would edit it, but I want to make sure which you meant.  This doesn't change my thinking on the matter.

I think you can normally think about similar pressures leading to extended-spectrum beta-lactamase (ESBLs) and  methicillin/oxacillin-resistant Staphylococcus aureus (MRSA).
Going to the core of your question:
"Currently, the reported mechanism of methicillin resistance in S. aureus is the production of a distinctive penicillin binding protein 2a (PBP2a), which exhibits low affinity toward β-lactams"
But to really read on it you need to back to Liu et al.
Again Todar's is a great source for a good broad reading on staph including MRSA.
Response to Edit [inclusion of full question]:
TSDR: The answer is C.
Let's break down the three options given in the question and learn about MRSA along the way.

a. its MIC is increased to methicillin, but not to penicillin

First, for people who may not know, MIC is short for minimum inhibitory concentration.  Simply, the MIC is a basic measurement of how much of any given agent is need to stop the growth of a bacterial colony.  Often we think of current medical antibiotics when thinking of MIC, but even simpler things like table salt and sugar have a MIC for a given species.  Thus this sentence is making the assertion that the bacteria found in the patent have an increased resistance to methicillin but not to penicillin.  This leads us to ask the obvious question:
Can Staphylococcus aureus (staph going forward) be methicillin resistant but not penicillin resistant?
This is a bit of a trick question, but let's break it down to the needed components: What is Methicillin, what is/are penicillin(s), and how are staph resistant to them.
First that it should be noted that penicillins can actually refer to a whole class of antibiotics which all use β-Lactam and the specific set of antibiotics:

benzylpenicillin (penicillin G), procaine benzylpenicillin (procaine
  penicillin), benzathine benzylpenicillin (benzathine penicillin), and
  phenoxymethylpenicillin (penicillin V). (from wiki)

It should be noted that more correct way to address the whole class of antibiotics would be β-Lactam antibiotics, not penicillins, and that if you wanted to talk about more specifically penicillin derived compounds you would be discussing penams.  For even further clarification, penicillin as drug most likely refers to benzylpenicillin, and for the rest of this answer I will use penicillin to refer to benzylpenicillin.
Thus we should think of penicillin as an early antibodic that work by preventing the dividing/genesis of cell walls and certain organelles via binding to penicillin binding proteins (PBPs).
Methicillin is also a β-Lactam antibiotic, and it's MOA is similar to penicillin.  It was developed/discovered after penicillin and was seen a answer to Gram-positive bacteria that were breaking down penicillin via β-lactamase.  Methicillian still works by binding to PBPs, but it escapes the bacteria's counter to penicillin.
This leads us to address how penicillin resistance and methicillin resistance commonly occur in staph.  First, many staph strains and other bacteria use β-lactamases to breakdown antibiotics so they no longer can bind to PBP's (1).  But methicillin is particularly suited by its side chains to not be degraded by β-lactamases.  In their ground breaking work on the subject, Hartman and Tomasz identified that methicillin resistance was not in the acquisition of a β-lactamase, but in a mutation in PBP's that prevented methicillin binding (2).  There they tested 4 strains of staph, two were methicillin resistant (MR), and two were methicillian susceptible (MS).  You will note that all but 1 didn't have β-lactamase activity, and where more susceptible to penicillin than methicillin (ibid).
BUT this does not mean that MR strains are not also penicillin resistant, instead it shows that the resistance can be independent of each other.  Therefore "A" is wrong because it tries to draw a correlation that is not there.  In reality many MR strains are also β-lactamase positive.
This also address the problem with "B."  While it is possible that a β-lactamase could bind to methicilin and lead to degradation of the antibiotic, the main mechanism of methicillin resistance is the mutation of PBPs (ibid, 3), in particular BPB2a (4, 5).
We are then left with the task of figuring out why "C" is the correct choice.  Indeed "C" is the given reason for the failure of "A" and "B," but we can still go deeper into how and perhaps why BPB2a mutated.
For that I think it is best that we turn back to Chambers' review of the subject.  Forgive my over quoting, but it's done so well there and the text is now open.

Methicillin resistance is associated with production of a novel PBP
  that is not present in susceptible staphylococci. Resistant strains of
  S. aureus produce an additional 78- kilodalton PBP (Fig. 1), termed
  PBP2a or PBP2' (assumed to be identical for the purposes of this
  review), that has a low binding affinity for beta-lactam antibiotics.

...

PBP2a is highly conserved. Limited proteolysis of PBP2a from unrelated
  strains of S. aureus (123) and coagulasenegative staphylococci (31),
  whether homogeneous or heterogeneous, generates remarkably similar
  peptide fragments.

...

Presumably PBP2a can substitute for essential PBPs when these have
  been saturated by drug and can perform the functions necessary for
  cell wall assembly (22, 122).

...

In some strains, PBP2a is inducible by beta-lactam antibiotics and its
  production differs according to growth conditions (34, 122, 125, 159).

Unfortunately, they didn't quite have the staphylococcal cassette chromosome mec (SCCmec) figured out at that point.  The genetics is quite complex.
How does MRSA genetically accomplish resistance?
As we already established, the resistance comes from the production of an alternate PBP, PBP2a.  SCCmec is interesting for several reasons.  First of all, it's much larger than a plasmid, and contains information for several genes.  That's why it's called cassette chromosome.  Further it normally incorporates into the same part of the genome in staph, in an area know as OrfX (6).  This means that even during horizontal transfer, that the cassette has to direct it's integration into the genome, which is exceedingly uncommon, or at least there are not many other know examples (7, 8).  This cassette can be spread horizontally between staph, and even with other species (ibid, 9).  Even if the integration site (integration site sequence, ISS) is slightly different, this specificity is carried out by cassette chromosome recombinases (ccr), wich are also on SCCmec (8).  This is carried out by ccr-medated recombination of the target chromosome, and further details on the process are considered outside the scope of this question.
The actual gene that encodes PBP2a is called mecA.  But as we mentioned above, PBO2a production can be induced and regulated.  It is likely less favorable to produce it in the absence of antibodies, and after serial passage of bacteria in antibiotic free broth, you find that PBP2a expression can drop drastically.  Therefore regulatory and other useful proteins encoded by SCCmec.  When placed in a β-Lactamase environment, MecR1 causes a single transduction cascade to start transcription of mecA (10).  Conversely, MecI provides a negative feedback loop to MecR1, and in the absence of β-Lactamase, will lead to the down regulation of mecA (ibid, 11).  The actual action of MecR1 is to cleave MecI, thereby remove the suppression of mecA by MecI.  I actually learned something new when reading the wiki on MRSA, but didn't do further research on the subject:

mecA is further controlled by two co-repressors, BlaI and BlaR1. blaI
  and blaR1 are homologous to mecI and mecR1, respectively, and normally
  function as regulators of blaZ, which is responsible for penicillin
  resistance. The DNA sequences bound by MecI and BlaI are
  identical; therefore, BlaI can also bind the mecA operator to
  repress transcription of mecA.

This represents the general pattern of resistance of MRSA, but there is a rich diversity in the particulars of how each strain manages expression.  Two of the main identifiers are how the mecA gene complex and ccr gene complex are configured (carriage).  The other two identifiers are the ISS and whether or not the ISS is repeated in the target chromosome (and how many times it's repeated) (8).  If we just consider the mecA and ccr carriage, then we get a great summary from IWG-SCC (ref 8):

The mec gene complex is composed of mecA, its regulatory genes, and
  associated insertion sequences. The class A mec gene complex (class A
  mec) is the prototype complex, which contains mecA, the complete mecR1
  and mecI regulatory genes upstream of mecA, and the hypervariable
  region (HVR) and insertion sequence IS431 downstream of mecA. The
  class B mec gene complex is composed of mecA, a truncated mecR1
  resulting from the insertion of IS1272 upstream of mecA, and HVR and
  IS431 downstream of mecA. The class C mec gene complex contains mecA
  and truncated mecR1 by the insertion of IS431 upstream of mecA and HVR
  and IS431 downstream of mecA. There are two distinct class C mec gene
  complexes; in the class C1 mec gene complex, the IS431 upstream of
  mecA has the same orientation as the IS431 downstream of mecA (next to
  HVR), while in the class C2 mec gene complex, the orientation of IS431
  upstream of mecA is reversed. C1 and C2 are regarded as different mec
  gene complexes since they have likely evolved independently. The class
  D mec gene complex is composed of mecA and ΔmecR1 but does not carry
  an insertion sequence downstream of ΔmecR1 (as determined by PCR
  analysis).

And

ccr gene complex.The ccr gene complex is composed of the ccr gene(s)
  and surrounding open reading frames (ORFs), several of which have
  unknown functions. Currently, three phylogenetically distinct ccr
  genes, ccrA, ccrB, and ccrC, have been identified in S. aureus with
  DNA sequence similarities below 50% (Fig. 2 and 3). The ccrA and ccrB
  genes that have been identified to date have been classified into four
  allotypes. In general, ccr genes with nucleotide identities more than
  85% are assigned to the same allotype, whereas ccr genes that belong
  to different allotypes show nucleotide identities between 60% and 82%.
  All ccrC variants identified to date have shown ≥87% similarity; thus,
  there is only one ccrC allotype. We suggest describing their
  differences as alleles by using previously used numbers, e.g., ccrC1
  allele 2 or ccrC1 allele 8.

All of this is nicely summarized in their table:
\begin{array} {|r|r|r|}
\hline
SCCmec ~type  &ccr ~gene ~complex  &mec ~gene  ~complex \\
\hline
I &1 ~(A1B1) &B \\
\hline
II &2 ~(A2B2)&A \\
\hline
III &2 ~(A3B3)&A \\
\hline
IV &2 ~(A2B2)&B \\
\hline
V &5 ~(C)&C2 \\
\hline
VI &4 ~(A4B4)&B \\
\hline
VII &5 ~(C)&C1 \\
\hline
VIII &4 ~(A4B4)&A \\
\hline
\end{array}
To sum up, methicillin-resistance is caused by the encoding of a novel PBP, PBP2a, along with other factors, which is both genetically stable and transferable via the use of SCCmec.
References:
(1) Pathak A et al. High prevalence of extended-spectrum β-lactamase-producing pathogens: results of a surveillance study in two hospitals in Ujjain, India. Infect Drug Resist. 2012;5:65-73. doi: 10.2147/IDR.S30043. Epub 2012 Apr 5. [Note that many of the great sentinel studies on drug resistant bacteria occur in the massive hospitals in India].
(2) B Hartman and A Tomasz. Altered penicillin-binding proteins in methicillin-resistant strains of Staphylococcus aureus. Antimicrob Agents Chemother. 1981 May; 19(5): 726–735.
(3) Liu, H. et al. Detection of borderline oxacillin-resistant Staphylococcus aureus and differentiation from methicillin-resistant strains. Eur J Clin Microbiol Infect Dis. 1990 Oct;9(10):717-24.
(4) Tawil N. et al. The differential detection of methicillin-resistant, methicillin-susceptible and borderline oxacillin-resistant Staphylococcus aureus by surface plasmon resonance.  Biosens Bioelectron. 2013 Nov 15;49:334-40. doi: 10.1016/j.bios.2013.05.031. Epub 2013 Jun 4.
(5) Chambers HF. Methicillin-resistant staphylococci. Clin Microbiol Rev. 1988 Apr;1(2):173-86.
(6) Huletsky A et al.  New real-time PCR assay for rapid detection of methicillin-resistant Staphylococcus aureus directly from specimens containing a mixture of staphylococci. J Clin Microbiol. 2004;42(5):1875-84. DOI: 10.1128/JCM.42.5.1875-1884.2004
(7) Schoenfelder SM et al. Success through diversity - how Staphylococcus epidermidis establishes as a nosocomial pathogen. Int J Med Microbiol. 2010 Aug;300(6):380-6. doi: 10.1016/j.ijmm.2010.04.011. Epub 2010 May 6.
(8) IWG-SCC. Classification of staphylococcal cassette chromosome mec (SCCmec): guidelines for reporting novel SCCmec elements.  Antimicrob Agents Chemother. 2009 Dec;53(12):4961-7. doi: 10.1128/AAC.00579-09. Epub 2009 Aug 31.
(9) Stürenburg E. Rapid detection of methicillin-resistant Staphylococcus aureus directly from clinical samples: methods, effectiveness and cost considerations.  Ger Med Sci. 2009 Jul 6;7:Doc06. doi: 10.3205/000065.
(10) Jensen SO and Lyon BR. "Genetics of antimicrobial resistance in Staphylococcus aureus". Future Microbiol 4 (5): 565–82. doi:10.2217/fmb.09.30. PMID 19492967
(11) Oliveira DC, de Lencastre H.  Methicillin-resistance in Staphylococcus aureus is not affected by the overexpression in trans of the mecA gene repressor: a surprising observation. PLoS One. 2011;6(8):e23287. doi: 10.1371/journal.pone.0023287. Epub 2011 Aug 2.

Clear answer and well summarised! Please, cover in more detail the SSCmec thing. You left out mecA gene which is located in SSCmec. Bacterial resistance to methicillin and related penicillins is mediated by acquisition of mecA that codes for a novel penicillin-binding protein, PBP2a, that has a low affinity for methicillin and related penicillins and cephalosporins. This is all what is covered in Murray Microbiology book.

@Masi Sure thing.  I didn't want to go into a tangent, you could probably write a whole dissertation on this.  I will update before the end of the bounty.

@Masi  Sorry about the delay, but I think that probably covers what you were looking for.  If you know how to better format that table, I couldn't get it to look right.

Acquisition of a new PBP (eg methicillin resistance in staphylococcus aureus), source Murray.
So I think the answer is C: change in configuration (mutation) of PBP, which can interpreted as acquisition of a new PBP.

I noticed that you still haven't edited your own awnser.  I think you mean to say the awnser is C.  I would like to point out that the alternate for of PBP, PBP2a is not really new, mearly has upregulated expression vs classic PBP.  Are you looking for information in how the binding site structure changed?  I want to make sure I'm adding the kind of clarity you are looking for.


text:
What are the best detection medias for cholera?
I heard this fact that you can use some [hypertriade] for vibrio cholera diagnosis which has compontents

sucrose (yellow)
mannose (yellow)
arabinose (do not ferment; stay dark pink)

I did not find this hypertriade agar on Google.
It reminds me of Egg Yolk Agar, but I think cannot be it because of the arabinose.
Otherwise, it seems to be similar.
What are the best detection medias for cholera?

I don't see how you could have a single medium that would simultaneously test for fermentation/non-fermentation of three different sugars. From the colours that you mention this is clearly based on a tetrazolium salt, but if all three sugars were present then two of them would be fermented and you would get a conversion to a yellow product, regardless of the inability to ferment arabinose.

@AlanBoyd I added an explanation what the hypertriad may refer to: there can be three selective media in one petri dish. I am not sure why they are using the word hypertriade or hypertriad. They seem to be using only sucrose, mannose and arabinose. Is there any collective name for such combination?

Is there a reason you wouldn't be using TCBS?  Why the "hypertriade" in the first place?  If you're designing a specimen screen, you might use 4 instead. I also, I've never heard the phrase hypertriade, and DDG/Google failed to teach me. Do you have a reference for that term?

@AtlLED Make that an answer and I will accept it. I do not know why the assistant was using the word hypertriade. I have no idea of the origin.

You should use Thiosulfate-citrate-bile salts-sucrose agar for the detection of all vibros, including cholera.  When cholera is presant, you should expect round, largish (not huge), yellow colonies.  This is the CDC recommended diagnoses method.
Again this question might be better phrased "what are the best detection medias for cholera," or "what plate screens should be conducted when vibros are suspected?"


text:
Genome Project Focusing on gene ADRB2?
I am not sure which project database to use UCSC or Ensembl for my asthma study about ADRB2 gene (Arg/Arg-16 genotype).
I am using the original Human Genome Project database at the moment.
However, I think Ensembl may be better suited for me.
Which genome database is good for Asthma research for Single Nucleotide Polymorphism (SNP variations)?
I am looking for something which has existing visualisation tools or one where you can easily write one yourself.

I don't understand what you're asking. Ensembl has subsections that let you look at a single genomes. The fact that the database has other genomes is irrelevant.  What are you calling the "original Human Genome Project"? Do you mean UCSC? What kind of data do you want to visualize?

I think it can be UCSC that was first out. Tools that give overview of the database and let me then focus on some sample.

There is actually no difference between the databases, as they use the same datasets. Only the way you can display and look at the data is different. I like Ensembl more, but this is a flavour. And I got a pretty good introduction to it.

@Masi, all of them do that, that's the point og a genome browser. Can you please edit your question and narrow it down? I still don't know what you need that neither the UCSC nor Ensembl offer you. The only way to choose between them is personal choice or specific tools provided but since you don't explain what you want to do, it's hard to help.

@terdon Thank you for feedback! I pickup the gene Arg/Arg-16 which I am browsing in infantile asthma.

I ask again, please clarify. Arg/Arg16 is not a gene, its a genotype; I think the gene you mean is ADRB2. You still have not told us what is missing from the tools you are using. You have not explained what exactly you want to visualize nor what exactly you are looking at. I am beginning to guess you are after SNP variations but I'm not sure. You mention vertebrates, does that mean you want to do a comparative analysis of some sort? Please [edit] and be more specific.

Thank you for helpful comments! I focused the question even more. Just ADRB2 and SNP.

So you are looking for a way to find mapped SNPs in the ADRB2 gene?

Yes. You are right.

If you are looking for variations in a gene, there are a few databases you an consult.
You can of course use the usual genome browsers, search for your gene and then select the variations listed. For ADRB2 this looks like this on Ensembl. If you plan to retrieve and compare data from different genomes/genes, I really recommend learning how to use Biomart, as this is a very powerful tool.
Then you can use specific databases or search engines, which only target SNP's. Examples would be: DBSnp and SPSmart (which queries different databases).

Very clear and excellent answer! Thank you for mentioning those tools! I am in the beginning of reviewing and learning them. :)

You're welcome. BTW: If you have the chance of participating in one of the Ensembl courses, do it. It is definitely worth the time.

I will do it when my studies go to Clinics phase.


text:
Can Rubella virus pass into brain stem?
B19 virus (about 20 nm) can; which I think is partially because of its small size; not sure of genomics has something to do with the passing. Rubella's (also called German measles) size is then again minimum 45 nm.
So I started to think if this virus can pass into the brain stem.
Can Rubella pass into the brain stem?
Some studies are made about Rubella associated hemolysis.
I think it is not related with this question at all.
Rubella is diffused along carbon dioxide from capillaries into the brain stem, this is my hypothesis.

What makes you think there is a connection between hemolysis (the breakdown of red blood cells) is connected to an infection of the brain?

@Chris Thank you for pointing out my not clear point out! I do not know what is the role of hemolysis with rubella in diffusion to brain stem. I cleared the confusion in the body.

It obviously can do that, causing a rubella encephalitis. A specialized form seems to be the "Progressive rubella panencephalitis", which is very rare with only 20 cases described since its first description in 1974.
About rubella encephalitis more papers are available, see these for a start:

Neurological aspects of rubella virus infection.
Mumps encephalitis: return with a vengeance.
Neurological Aspects of Rubella Virus Infection

Exactly! I have this disease also in my notes. I think it can be caused also by Measles encephalitis. I think Mumps encephalitis cannot cause the disease because it is too big. The disease is only caused by some Measles virus variant and rubella. Both lead to demyelination in CNS progressive degeneratively and ending in exitus letalis.


text:
Latency to audition in human beings?
On average, in a human being with no neurological deficits, how long does it take for a sound which is sensed in the ear to reach the cortex?
Which brainstem structures are most responsible for the delay?
(I'm interested in things like the effect of the Olivary n.)

There are several ways to infer into the propagation delays of auditory system in vivo that is applicable to humans (i.e. leaves the subjects intact).
One of them is so-called ABR that stands for Auditory Brainstem Response. As it is clear from its name this method allows you to derive the brainstem response to an auditory stimulus (so, you can track the auditory pathway up to its input into thalamus), but its resolution is so fine that you can separate single components ("waves") for the following path segments (from Wikipedia):

Wave I – generated by the peripheral portion of cranial nerve VIII
Wave II – generated by the central portion of cranial nerve VIII
Wave III – generated by the cochlear nucleus
Wave IV – generated by the superior olivary complex/lateral lemniscus
Wave V – generated by the lateral lemniscus/inferior colliculus

So, it takes only 10 ms for the signal to reach the input into thalamus. This correlates well with some auditory signal based activities, like startle reflex, which was also shown to have about 10 ms latency.
I tried to search for some electrophysiological recordings from auditory cortex (temporal lobe) paired with auditory stimuli, but the first paper I came accross that is available for free (and which I can also link from my answer) is this work done on monkeys.
If you look at Figure 1:

This is the results from multiunit recordings and you see that the initial activity in the cortex starts approximately 20 ms after the stimulus onset with a short activity pattern, followed by some short break and then longer period of activity with broader frequences spectrum.
In my opinion the delays in signal propagation are not due to complex signal processing in the olivary nucleus or any other brainstem structures, rather they are due to electro-chemical transformations in CNS synapses.
The initial arrival of the signal into the cortex does not mean the perception of the sound, it definitely takes hundreds of millisecond until the conditioned cortex-mediated response to this stimulus.


text:
How do the pharmacodynamics of the NSAIDs differ and are there "resistant" COX phenotypes?
I know that the non-steroidal anti-inflammatory drugs (e.g., aspirin, ibuprofen, naproxen) affect the enzymes cyclooxygenase (types I and II).
Is there any difference in the degree to which these drugs manipulate/inhibit the enzymes (I assume their affinities for COX-1 and COX-2 are at least somewhat different)?  Is there any evidence as to whether the the NSAIDs collect in certain areas of the body in a compartmental fashion?
Are there differences in fat solubility, etc., between the different drugs?
Finally, are there any known phenotypes of COX-1 and COX-2 enzymes that are present in the general population that affect the ability of these drugs to act?

What do you mean by collect in certain areas of the body in a compartmental fashion?

@Masi Thanks for your answer!  I meant whether there were differences in fat solubility, etc., between the different drugs.

Thank you for your comment! I will look for the fat metabolism thing next week. Your updated question will have completely different answer than the old one.

This is a draft.
How do the pharmacodynamics of the NSAIDs differ - -?
Merck's manual ch. 36 to start little bit at an introductory level:

The anti-inflammatory activity of the NSAIDs is mediated chiefly
  through inhibition of biosynthesis of prostaglandins (Figure 36–2).
  Various NSAIDs have additional possible mechanisms of action,
  including inhibition of chemotaxis, down-regulation of interleukin-1
  production, decreased production of free radicals and superoxide,
  and interference with calcium-mediated intracellular events.  Aspirin
  irreversibly acetylates and blocks platelet cyclooxygenase, while most
  non-COX-selective NSAIDs are reversible inhibitors.

and see the coming answer below.
These questions should be answered together.
To split them can be confusing.
Is there any difference in the degree to which these drugs manipulate/inhibit the enzymes (I assume their affinities for COX-1 and COX-2 are at least somewhat different)?
Please, see ch 1.03.3 in Comprehensive Natural Products II: Chemistry and Biology: 10 Volume Set:

and their conclusions about the structure

and please, see the whole chapter of the book, since its about the topic - and I think good one.
From Katzung et al.

Selectivity for COX-1 versus COX-2 is variable and incomplete for
  the older NSAIDs, but many selective COX-2 inhibitors have been
  synthesized. The selective COX-2 inhibitors do not affect platelet
  function at their usual doses.
On the other hand, selective COX-2 inhibitors may increase the
  incidence of edema and hypertension.
To varying degrees, all newer NSAIDs are analgesic, anti-inflammatory, and antipyretic, and all (except the COX-2- selective
  agents and the nonacetylated salicylates) inhibit platelet
  aggregation. NSAIDs are all gastric irritants and can be associated
  with gastrointestinal ulcers and bleeds as well, although as a group
  the newer agents tend to cause less gas- trointestinal irritation than
  aspirin.

In short, there must be differences to which these drugs manipulate/inhibit the enzymes.
Please, see

Selinsky BS, Gupta K, Sharkey CT, Loll PJ. Structural analysis of
NSAID binding by prostaglandin H2 synthase: time-dependent and time
independent inhibitors elicit identical enzyme conformations. Biochemistry 40, 5172–5180 (2001).

Defining the COX Inhibitor Selectivity of NSAIDs: Implications for Understanding Toxicity. Expert Rev Clin Pharmacol. 2010;3(6):769-776. And see the chapter Expert Commentary which locates at the end of the publication there:

Not withstanding the caveats on the merit of IC50 values, in vitro
  analyses of COX-1 and COX-2 selectivity of NSAIDs has driven the
  concept that inhibition of COX-1 explains the predominant reduction in
  synthesis of mucosal protective PGs and hence gastrointestinal
  toxicity of NSAIDs relative to COX-2 inhibition, which plays a role in
  ulcer healin

Merck's manual chapter 36

The discovery of two cyclooxygenase isoforms (COX-1 and COX-2) led to
  the concept that the constitutive COX-1 isoform tends to be
  homeostatic in function, while COX-2 is induced during inflammation
  and tends to facilitate the inflammatory response. On this basis,
  highly selective COX-2 inhibitors have been developed and marketed on
  the assumption that such selective inhibitors would be safer than
  nonselective COX-1 inhibitors but without loss of efficacy.

Inflammatory processes are expressed by both COX-1 and COX-2 differently.
This means that a change in the cell membrane expresses lysosomal enzymes differently:

The cell damage associated with inflammation acts on cell membranes to
  cause leukocytes to release lysosomal enzymes; arachidonic acid is
  then liberated from precursor compounds, and various eicosanoids are
  synthesized.

Also, the cyclooxygenase (COX) pathway of arachidonate metabolism produces prostaglandins, which have a variety of effects on blood vessels, on nerve endings, and on cells involved in inflammation. (See Merck, ch. 18)
I like the Figure 36.2 in Merck's manual.
To better answer your question, one could label the arrows there with relevant enzymes in each processes and compare those between COX-1 and COX-2 and relate to corresponding publications (only few existing!).
Adrenaline and other compounds activate the cyclooxygenase pathway, COX-1 pathway for instance, and the conversion of arachidonate to PGs and TXs. [2, p. 67]
The classic law of mass action allows to describe the reversible binding:
\begin{equation}
    [Protein] + [L] \rightleftharpoons^{k_{1}}_{k_{-1}} [Protein-L]
\end{equation}
where $L$ is ligand, Protein-L the protein-ligand complex, $k_1$ the rate constant of the forward reaction, while $K_{-1}$ the rate constant of the reverse reaction.
This fine regulation differs between COX-1 and COX-2 at enzymatic level regulated by cytokines.
COX-1 becomes only little activated in inflammation, in comparison to COX-2.
COX-2 is present in macrophages (chronic inflammation! - cytokines), fibroblasts, endothelial cells, synovial fluids, and chondriocytes.
[A]re there “resistant” COX phenotypes?
I have not heard about this that there would not be.
There are so many components in PGHSs which can develop resistances.
[A]re there any known phenotypes of COX-1 and COX-2 enzymes that are present in the general population that affect the ability of these drugs to act?
Please, see for the phenotypes of COX-1 here, while about COX-2 much less has been research, see here - no known phenotypes, see this.
Please, note also that COX has at least two isoforms: COX-1 (PGHS-1) and COX-2 (PGHS-2).
COX-1 phenotypes

176805, here

Is there any evidence as to whether the the NSAIDs collect in certain areas of the body in a compartmental fashion?
No.
Each disease has its own characteristics.
Gout, for instance, has swelling of syvovial joints and usage of NSAIDs with COX-2.
My professor of abdominal surgery answered to this question directly - impossible to answer generally which I agree with her. (17.10.2014)
I think the OP has in mind some antibiotics which concentrate in some parts of the body (such as 1st generation quinolones concentrating in the renal tubules and bladder, thus exerting local antibacterial effect).
There is no similar effect with NSAIDs.
Instead, NSAIDs have local and systemic effects, not because they are concentrating in some parts of the body, but because they have several mechanisms itself.
Please, see this thread about Effect of NSAIDS on stomach.
Are there differences in fat solubility, etc., between the different drugs?
Fat burner - of course, there are differences in fat solubility between different NSAIDs.
Please, see this publication Solubility of Nonsteroidal Anti-inflammatory Drugs (NSAIDs) in Aqueous Solutions of Non-ionic Surfactants.
I will update this part next week more.
Other sources

Basic and Clinical Pharmacology, 11th edition, 2009, Bertram Katzung.
My notes during Biochemistry classes in Tartu 2011-2013


text:
How do fibers control muscles?
My professor says

Nervus troclearis IV somatomotor fibers supply musculus obliquus superior.

and similarly for nervus oculomotorius III

Nervus oculomotorius postganglionic fibers supply musculus ciliaris, m. sphincter pupillae.

I understand the verb "supply" as "stimulate" or "allow signal pass from the tract to the muscle that contracts or flexes". However, fibers must have some other functions too. So the verb supply seems to be a general term for these functions.
How do fibers control the muscle?

I'm of the opinion that this question is either too localised or even off-topic in its present form.  Perhaps consider rewording it to sound less like a use of english question - "what is the link between these nerves and muscles" or similar?

I guess that was partly my fault from my edit.

@DanielStandage I wouldn't say that :)  Anyway it's in better shape now, I've reversed my down-vote.

I still think it needs more explanation. Are you looking for the answer to how action potentials are carried along motor neurons or how neuromuscular junctions work or both of the above?

@Kevin so the thing includes the two things. I know about the first one that myelin is used in some cases as a resistant. I know about the last one that there are transmitter substances like acetylcholine that is released from the end of the axon to the extracellular space that activates the action potential in some other cells by attaching to receptors of other cells. So there is a synapse going on between neurons. - Those things should apparently apply to the above examples. However, not sure how m. ciliaris is in connection with m. sphincter pupillae. Fibers activating muscles in sequence?

Read "supply" as "carry action potentials to." When the action potential reaches the junction with the muscle (i.e., the neuromuscular junction), neurotransmitters are released into synapse. A similar membrane depolarization occurs on the muscle cell, ultimately leading to contraction.
Nerves visible to the naked eye are actually bundles of individual axons (hundreds, thousands, or tens of thousands of axons). Nerves have the appearance of branching because the individual axons that travel to muscle fibers don't all go to one muscle.
For example the oculomotor nerve branches:

So what you see as the oculomotor nerve is really a collection of neurons. Some of these carry action potentials to the ciliary muscle and some to the sphincter pupillae. These are the parasympathetic components. There is a completely separate set of neurons (but still contained in the same nerve) that carry signals to the extraocular muscles.
This is really basic material that your professor should have explained to you.

Can you distinct the parasympathetic components of the nervus oculomotorius from a picture by eye?

They would be indistinguishable to the naked eye. You could only tell the divisions by where the (very tiny) branches go to.


text:
What are differences between formation of embryonic disc in chick and mammal embryo?
Exam question which got lowest average points in my university: 1/5 average.
No markscheme available so my attempt below.
I assume that embryonic disk prefers to germ disk such that Formation prefers to only to the 3rd developmental week because of the Wikipedia fact.
I also went through the points during 2nd week of development and did not notice major differences. So let's consider only the 3rd week:

Formation of the primitive streak
Genesis of the germ layers
Genesis of the notochord
Location of the epiblast cell target and the development of the primitive streak
The bilaminar membranes
Evolution of the mesoblast
The intraembryonic coelom
Induction of the neural plate – neurulation

The following differences are based mostly on Gilbert's Developmental Biology 9e -book.
Other Differences which seems to at least start at the 3rd week of development

Chick meroblastic cleavage, human holoblastic. TODO do not know how that causes differences yet during the 3rd week.
Chick has yolk, human not so human placenta development and implantation. Chick dependent on yolk nutrients, human not.
Human embryo gets mother nutrients through placenta.
Chorion formation and finally from it the fetal portion of the placenta.
Chorion also includes the uterine cells to form the maternal of the placenta, the decidua.
The decidua will come rich in the blood vessels that will provide oxygen & nutrients to the embryo.
Human oviduct expansion to the uterus.
Chick embryo externally developing from the mother, human not. Chick egg is telocithal with a small disc of cytoplasm: blastodisc - sitting atop a large yolk. The yolk, eggs of birds undergo discoidal meroblastic cleavage. Cleavage occurs only in the blastodisc which is about 2-3 mm in diameters & is located at the animal pole of the egg. The first cleavage furrow appears centrally in the blastodisc; other cleavages follow to create a single-layered blastoderm.
The cleavages do not extend into the yolk, cytoplasm, so the early-cleavage cells are continuous with one another & with the yolk at their bases.
One chick hypoblast streak, human multiple. Chick must have some control mechanism.

What are the differences between formation of embryonic disc in chick and mammal embryo?

Embryonic disc forms on top of yolk during cleavage on chicken embryo, while between amniotic sac and yolk sac inside blastocyst after implantation on human embryo.

Some further processes take place on and in the embryonic disc: specifically these here during the week 3.
Embryonic disc formation includes still during the 3rd week of development:

Formation of the primitive streak
Genesis of the germ layers
Genesis of the notochord

Formation of the primitive streak: The process of primary neurulation appears to be similar in chick and mammalian. The embryonic disc becomes oval and then pear-shaped, the wider end being directed forward. Near the narrow, posterior end, the primitive streak makes its appearance and extends along the middle of the disc for about one-half of its length from migrated ectoderm cells.

Genesis of the notochord: “The notochord extends beneath the neural tube from the base of the head into the tail.” - As the mesoderm develops between the ectoderm and endoderm it is separated into lateral halves by the neural tube and notochord.
Figure 2: Neurulation. NB the use of neural groove is correct. Notochord is below neural groove. - Genesis of germ layers here: from a flat thing to a developed one.

Figure 3: Genesis of notochord and primitive streak. Yolk-sac surrounds notochord and primitive streak.


text:
Substrates of cytochemical reactions in this immunostaining
Expression of extracellular protein Laminin 9 alpha-4 chain in human skeletal muscle.
Indirect immunostaining with HRP immunostain marker. Ob.x40.
I have unsuccessfully searched NCBI -database, JSTOR and other major Biology databases for an answer. This suggests to me that I do not understand what is going on.
1. What are the substrates of above cytochemical reactions for the given immunostaining above?

I need to give a simpler question where I apparently know the reaction exactly, since it is possible that people cannot answer the above question.
Mitochondria in Hep-2 cell line cells. Cytochemical test for mitochondria specific enzyme NAHD dehydrogenase. Ob.x40.
2. What is the substrate of the cytochemical reaction?
My answer:
The reaction of NADH dehydrogenase is:

NADH + H+ + CoQ → NAD+ + CoQH2

Substrate: CoQ

I'm having a hard time understanding this, it looks like some context is missing. If you're posting homework, please provide the full text of the problem and show what you've tried so far and what exactly you don't understand.

@MadScientist: Please, see pages 3 and 4 of the file: http://dl.dropbox.com/u/175564/Practical%20works%202011-2012.pdf

For my benefit can I ask why the in and out are included in the equation?

@Rory Because I was stupid when copy-pasting the given equation without deleting them, since we do not need them in my opinion. Right?

@Rory I removed 4H from the both sides. Correct now?

@Masi Looks fine :)

It's hard to understand the question, but in any immunocytochemical staining such as the above, you have two different types of reactions:

the antibody binding to the target (in this case, some laminin)
the peroxidase-based colorimetric reaction with DAB. DAB (3,3'-diaminobenzidine tetrahydrochloride) is oxidized in the presence of hydrogen peroxide to form a brown precipitate, which becomes the stain.

The fact that is an indirect immunostaining implies that you have a non-conjugated primary antibody against laminin and a secondary antibody against the Fc part of immunoglobulins of the species in which the first antibody was raised. This secondary antibody will be conjugated with HRP (horseradish peroxidase, the enzyme responsible of generating the peroxides that will oxidize the DAB).
For a more complete reference of immunocytochemical stainings, you can read: http://www.ihcworld.com/_books/Dako_Handbook.pdf

Thank you for your answer! Need to read the book in my Christmas holiday.


text:
What is the Giemsa staining of chromosomes?
I got the question in my exam and wrote the following and I do not understand what is wrong in it:

Giemsa staining is a staining method to stain particularly malaria and other parasital diseases. G-bands occur because Giemsa stain
  consists of A,T rich material i.e. poor gene such that dark and white
  bands occur. Each chromosome has an unique reaction to Giemsa staining
  so G-bands occur.

0 points. I do not understand what's wrong with it, since in their comments about the same question in my first exam they wrote also the extra questions: What are G-bands? How are they formed and why? This time I answered the given things and got zero mark.
Probably, the mistake was that I did not answer to the question in the scope of medical Biology in some way. However, I am not exactly sure what it is exactly.
How would you answer to the question when you know that the course was about medical biology?
Please, add the tag Giemsa.

Giemsa is too specific for its use as a tag. Staining and Histology are enough. Maybe Karyotype?

I suggest you explain downvote.

Giemsa is not a particular methid to stain malaria or any other parasite. It stains DNA. As such, it can be used to stain any DNA-containing organism, or, in other words, any known cell.
Regarding its particular use in chromosomal banding, you can refer to many online resources, such as this one of the University of Washington:

Chromosomes in metaphase can be identified using certain staining techniques, so called banding
(...)
G-bands are most commonly used. They take their name from the Giemsa dye, but can be produced with other dyes. In G-bands, the dark regions tend to be heterochromatic, late-replicating and AT rich. The bright regions tend to be euchromatic, early-replicating and GC rich.

Very well written. - - My attempt of a summary: Staining reveals structural features of the chromosomes in metaphase by banding. Giemsa staining offers better resolution of individual bands of chromosomes along the length of the whole chromosome. It stains DNA to heterochromatic (dark) and euchromatic (white) regions resulting into G-bands, called so because of the dye Giemsa, used in staining historically first, but can be stained also with other dyes. It stains any DNA-containing organism, or, in other words, any known cell. Analysis involves the karyotyping of banded metaphase chromosomes.

Is there any other staining methods for other phases than metaphase of chromosomes? - Is it useful to stain unreplicated daughter chromosomes after metaphase? It is probably harder to do it, since the daughter chromosomes are not in a line, than in staining during metaphase.

@Masi in any other phase of the cell cycle, the DNA is much less condensed (called chromatin) and basically all DNA is intermingled, rendering a much more homogeneous staining. You still see regions of condensed chromatin, but it's impossible to identify individual chromosomes. You may do some (very limited) in situ hibridization, but again it's much more informative when cells are in metaphase.

I need one clarification. Does Giemsa staining of chromosomes stain the DNA and proteins i.e. whole chromosomes? Or does it stain only DNA, not proteins?

It seems that Giemsa staining specifically stains DNA. Sometimes it seems that some proteins are staining but the purpose is not to stain them.

Probably they want something like from here:

For differentiate nuclear and/or cytoplasmic morphology of platelets,
  RBCs, WBCs and parasites. In wright- and Giemsa-stain: the cytoplasm
  appears blue and the nucleus is relatively large, eccentrically
  located and red. The distinct, rod-shaped, red-staining kinetoplast (a
  specialized mitochondrial structure) contains extranuclear DNA
  arranged as catenated minicircles and maxicircles.

In my opinion, the question is not exact if they want the above thing. It should have been: What is the Giemsa staining of chromosomes morphologically? if the above thing correct.
It was the first medical biology course so answer should be from it.


text:
Why does the arch of aorta coils?
My study materials use the word vesselcompression chamber of aorta to emphasize aorta's elastic property.
The arch of the aorta only coils, not its straight part.
I think the reason why the arch coils is the elasticity of aorta (artery) is high.
If the elasticity is too low, then the aorta is more stiff.
This means that heart has to work harder so higher systolic pressure and lower diastolic pressure.
Why does the arch of the aorta coils?

It's not clear to me what you mean by "coils". The aorta itself does not coil. Except for the arch, it's rather straight. Are you asking about the orientation of collagen and elastic fibers in the wall of the aorta?

@kmm This was the question which I got. It probably refers to the fact that it coils very little, exactly in the arch. Yes, I think the coiling of aorta can refer to the orientatino of collagen and elastic fibers in the wall of the aorta.

So if that is the case, then can you rephrase or narrow down your question?

@kmm I narrowed to question to the arch.

@Masi - I'm still confused by "coils." The aorta, as you said, is an elastic artery, and has many layers of smooth muscle and elastic fibers in the tunica media. Don't you mean: "if elasticity is low, then the aorta is stiff"? It requires high elasticity to help maintain a higher diastolic pressure.

@jello The topic is related to Pressure in Aorta and its characteristics. I do not understand why arch of aorta coils yet.

The main question can be answered in a very dumb way: because the lower part of the body also needs blood... and this configuration is the surest way of doing that because of reasons given below (among many others, I am sure).

If you want an anatomical reason, well the most pertinent one would be that embryologically, the heart and vascular system are derived from a single straight tube, that then begins contracting and folding over itself to form the heart chambers, the aorta, and the pulmonary trunk.
If you want a physiological explanation, the aorta curves slowly because it is a point of the circulatory system where pressure is high. Apart from the fact that sharp kinks would cause a massive and useless loss of kinetic energy on blood flow from shear stress over the aortic walls (and therefore more heart workload), the induced shear stress would also damage the aortic walls much more quickly than in the actual configuration.

The third reason is just theory on my part, but it seems the vascular system is designed by priorities: you could imagine a system with two aortas. One for the upper body going up, and a second going down. However, such a configuration makes it mechanically impossible to balance perfusion to the organs, and especially ensure brain perfusion. For example, how would the body compensate if the upper aorta got clogged while the other stayed wide open? The single aorta configuration allows the heart to adapt to such mechanical perturbation scenarii using, for example, left ventricular hypertrophy.
However to add to some elements of your question:

the reason of the aortic coiling has certainly very little to do with elasticity and the vessel compression chamber principle.
Higher elasticity means the aorta is less stiff, not more.
When the aorta gets stiff (elasticity decreases) as it is often the case with age and calcification of the aortic walls, it is correct that the heart will need to work more, that systolic pressure will get higher, and diastolic pressure lower. This gives the classical clinical symptom of "cannonball" or "gunshot" pulse

Excellent answer! Thank you! Can you provide me more information about the gunshot pulse. It reminds me about one case where the insulin secretion is like cannonball, here described: http://biology.stackexchange.com/q/17466/86

The other way of rejecting the two-aortic system away is the impossibility of having atrophy in the heart, I think. The cell size of the heart cannot decrease. I have listed some factors here what it would require http://biology.stackexchange.com/a/16928/86


text:
I need help identifying a completely unknown plant for my biology class
I know two things about this plant
1 is that it does not need to be watered for a long time because it has been able to survive in my schools greenhouse for quite some time without water and 2 my teacher says she "thinks" it blooms purple or pink flowers.
Thank you in advance for any help given!

Appears to be a succulent of some sort?

Any information on where it's native to?

I'm no expert on plants but it could be a kalanchoe. That's based mainly on the leaf characteristics and size.

There's some 120 or so species mainly originating from the old world. These are quite drought tolerant as yours seems to be. They are a common houseplant and there are ways to stimulate reflowering so that also makes it a good candidate.
Image source.

Awesome!! How is this done? Do you just happen to know them or you enter the characters or something in a key? Like, what is the std approach when you have no clue and youve got to identify?

@rg255 - JMusser will not get the ping unless he's posted in the thread. You might want to ping him in chat.

@Polisetty just persistence and searches!

Looks like a Kalanchoe to me, too! To answer @Polisetty 's question, you might go about identifying this by noting that it is a succulent ('juicy' leaves and does not need to be watered frequently), that it's opposite-leaved, that the leaf margins are jagged (I suppose maybe 'crenate' specifically), and that it has red flowers. This isn't going to help you much in using a botanical key, but might give you a start in google image-searching...

I was thinking of Sedum spectabile, another member of the Crassulaceae. But maybe Kalanchoe is better. @Polisetty Try to make it flower!


text:
Are plants really oxygen neutral?
This accepted and most upvoted answer to the question Does grass alone produce enough oxygen for life? claims that plants are oxygen neutral:

Plants are oxygen neutral The question wording is a bit misleading, as
  – surprise – plants do not produce oxygen. They produce oxygen only as
  long as they are growing, binding carbon in its mass. In long term all
  plants are oxygen neutral, as all oxygen which is created by them is
  again consumed when they dissolve, burn or are eaten, as carbon stored
  in them reacts with oxygen back to CO2. The more correct view how to
  describe this is not that plants produce oxygen, but that they store
  carbon.

I realize that a huge portion of our atmosphere's oxygen was produced by Phytoplankton, but the idea that plants produce zero net oxygen seems absurd to me. Is the information provided by that answer scientifically accurate? Please explain.

Plants produce oxygen throughout their lifetime by photosynthesis. If you look in a VERY long time period (many generations), then yes plants are oxygen neutral.

Plants are oxygen generators.  Plants plus decomposition (i.e. the whole system, plants plus bacteria and fungi and fire and cows and termites) are oxygen neutral. So the statement is literally wrong, but may be functionally correct in the current environment.

@iayork  Could you turn your comment into an answer?

This question seems to hinge on the exact definition of "oxygen neutral". So when asking it, you should say which definition you are interested in.

Plants are oxygen generators. Plants plus decomposition (i.e. the whole system, plants plus bacteria and fungi and fire and cows and termites) are oxygen neutral. So the statement is literally wrong, but may be functionally correct in the current environment.

Photosynthesis basically means 6 CO2 + 6 H2O --> C6H12O6 + 6 O2
Combustion/decomposition means the reversal... C6H12O6 + 6 O2 --> 6 CO2 + 6 H2O
Sequestering carbon dioxide is only temporary. However, the trees' reduction reaction provides us animals with that sugar and oxygen to burn. Without sugar and oxygen, practically all animals on earth would die. The trick to staying ahead of the curve for us now is to sequester more carbon and oxygen than nature can provide (for less money than it costs to dig for oil)... because it just so happens that we are pretty much consuming all the carbon and oxygen that farming plus living plants can supply, plus the fossil oil sequestered over millions of years.
Will grass be enough? No... neither the rainforest nor the algae in the ocean will be enough to offset the human over-population. We are burning far too much, far too fast for plants to keep up (naturally).

But to more directly answer the question, a 650-square-foot area of grass produces enough oxygen to sustain an average human adult's needs, whereas rainforests actually consume about the same amount of oxygen as it produces. Even though the rainforest has the highest rate of photosynthesis per unit area... it is primarily consumed (in balance) with the decomposition by the animals and microorganisms that live in it.
Or if you compare grassland to a regular forest, another way of conceiveing this is to say that a field of grass will generate more mass per year than a forest of equivalent area.
What about oceans? Well, they cover 71% of the earth and the estimated O2 production is between 50% and 85% (in the atmosphere). Since the ocean is basically able to provide about the same amount of O2 as land (plus the requirement of the sea animals), then you really do have O2 production from the ocean.
So let's just compare the star players, grass and phytoplankton. Well, phytoplankton are kind of difficult to grow in a lab and corn or wheat could be considered grass. So let's actually consider other kinds of algae and grain instead.
Without going too far in depth, some companies are claiming to be able to produce over 8 million gallons (or about 60 million pounds) of oil per acre from algae. That's a total slam dunk in the face of grass... even if they are just bragging (by a factor of 1,000). Algae fuel is the reason that bioreactors are "all the rage" right now (a veritable green gold rush), and companies are cropping up everywhere. Of course, genetic engineering has something to do with the numbers... but even if you compare algae with (genetically engineered) corn or canola, you are talking about a measly 150 gallons per acre give or take 20%. And corn definitely produces more weight (5 tons of seed plus another say 5 tons of cobs and stalks) than wheat (about 1.5 tons of seed, and about 1.1 tons of straw) per acre.

This is a bunch of interesting information for sure, but I don't think it answers the question.

@Roland it completely answers the questions by the OP! I'm totally stunned by your comment!

I believe the question was "do plants produce oxygen" + how to explain the quote from Skeptics SE, and I think the answer is basically given in @iayork's comment above. CO2 emissions / sequestrations and biofuel production are different issues I would say.

@Roland CO2 emission, sequestrations, and biofuels are the answer for the question do plants produce oxygen... and the quote from the skeptics SE... that plants are net zero. The first sentence of my answer is photosynthesis = combustion in reverse. Oil is sequestered carbon ultimately from photosynthesis. The weight of the plant is the measure of captured carbon. Oil is the most reduced form of carbon. Humans are currenly burning more O2 and reduced carbon than plants are producing. When we've burned it all it will equal zero. Until then, there's still sequestered carbon/oil on earth.

@Roland Plant weight (mostly from sugar and oil) is proportional to O2 production. When it is burned or decomposed the process is reversed. As noted in the answer of the skeptic SE, "The more correct view how to describe this is not that plants produce oxygen, but that they store carbon.". Although this is a bit simplistic, storing or sequestering carbon, means a (temporary) net production, which animals use and burn, digest, or otherwise decompose to live. As long as plants produce, animals have food and air. Tree's have produced... and fossil oils exist... but we are rapidly burning out.


text:
What unicellular eukaryotes reproduce sexually?
By sexual reproduction I am referring to, at least, gametogenesis or mating bridges. I was previously under the impression that unicellular organisms did not reproduce sexually at all.
So far the sexually reproducing unicellular eukaryotes I am aware of are yeast, diatoms, malaria-causing Plasmodium and some diplomonads.

Your definition of simplest is not exactly exclusive.

Huh! According to this article it is possible that sexual reproduction is the standard in eukaryotes: https://ittakes30.wordpress.com/2011/04/12/rewriting-the-history-of-sex/

This addresses your original question of "simplest" versus smallest. I'm not sure of sizes.
Investigate diplomonads: https://en.wikipedia.org/wiki/Diplomonad Most notable among them is Giardia: https://en.wikipedia.org/wiki/Giardia
These critters are primitive enough to lack Golgi and their version of "mitochondria" are substantially different enough (not synthesizing ATP) to be called by another name, mitosomes. Most have two nucleii and were not even thought to reproduce sexually  until relatively recently


text:
What is recemose inflorescence?
In recemose inflorescence

Main axis continues to grow,
The flowers develop in acropetal succession ,
Opening of flower is centripetal

But according to definition

Acropetal succession : flowers opening in succession from base to apex
Centripetal : the younger flowers are towards the centre and the older towards the outside...

I can't understand that if lower flowers or flowers towards centre open first then they should be older but according to above statement flowers at base are younger. Is there other concept that I don't know?

Inflorescence is a flowering shoot that bears more than one flower. There are two types of inflorescence Cymose and Racemose. Of the two types of inflorescence Cymose inflorescence is more primitive and Racemose is derived. (Parkin 1914)
Racemose
In this type of inflorescence the main axis does not end in a flower, but it grows continuously and develops flowers on its lateral sides in acropetal succession (acropetal (adj.) - of leaves or flowers; developing or opening in succession from base to apex ).
Acropetal sucession is observed in raceme, the simplest racemose
inflorescence.

Now Capitulum or Head, it is another type of racemose inflorescence in which

the main axis or receptacle becomes suppressed, and almost flat, and the flowers (also known as florets) are sessile (without stalk) so that they become crowded together on the flat surface of the receptacle. The florets are arranged in a centripetal manner on the receptacle, i.e., the outer flowers are older and open earlier than the inner ones.

In the following L.S. of sunflower you can see the disc florets developing/opening in centripetal manner.

P.S. I'm not a botanist but a candidate of B.Sc Zoology. I had Botany as my additional subject so I answered it from my knowledge.

I'll add more information as soon as I'm free.


text:
How large is the range of 'same origin' when determining whether two organs are analogous or homologous?
The pectoral fins of a whale and a shark. Are they analogous organs?
I was looking at this question, and I saw that the two answers defined the range of 'same origin' differently. One said that sharks and whales have the same origin as jawed animals, (therefore they are homologous) and the other said that they had different origins, namely cartilaginous fish and mammals(therefore they are analogous). Now here's the question.
How large is the range of 'same origin' when determining whether two organs are analogous or homologous? Is it as large as a Kingdom or a Phylum? Class? Order? Family? Or is there another criterion?


text:
Owl identification. Winter in Haliburton, Ontario, Canada
Is this owl a 'Great Grey Owl' or 'Barred Owl'? I'm thinking a Great Grey because it was quite huge - about 1.5 to 2 feet tall.

Cross-posted on The Great Outdoors

That is a nice picture of a Barred Owl. The heavy well-separated streaks on the breast and eye color (dark vs. yellow) are both distinctly different from that of the Great Gray. The markings in the facial disk are also distinctive — e.g. the fine even lines in the Great Gray vs. the blurry, more disordered pattern in the Barred. (Also Great Gray Owls are even bigger: 60-80+ cm long vs. 40-50 cm for Barred Owls.)
An excellent resource for identifying North American birds is the Cornell Lab of Ornithology's All about birds site. That link is to their comparison between these two species.

I agree. Strix varia (barred owl) vs larger, greyer, Strix nebulosa

Cornell has a great phone app, too, btw, to identify birds by sound. Its recognition accuracy is impressive.

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


text:
Why do cockroaches and flying beetles survive high levels of radiation?
Apparently it's a fact that cockroaches survive nuclear radiations.
How can they survive this?

I'm puzzled by your comment that humans are invulnerable to insecticides. Dosage is key; organophosphate poisoning is pretty common (and it is a pretty common insecticide.)

They survive radiations because of their slow cell replication, Humans are NOT invulnerable to pesticides at all. Most pesticides will have really negative effects on humans, and can cause deaths in certain concentrations.

Cockroaches have slow cellular replication rates and radiation is known to be the most dangerous to replicating cells, thus making cockroaches (and several other insects) more resistant to radiation than us, but not immune.
This was the subject on a Discovery episode of MythBuster


text:
Is Near-infrared focused light safe for your eyes?
I found a new product, but I'm afraid it's not safe. Can you help me understand what the safety limits are when it comes to near-infrared light focused on your eyes is?
I'm assuming the wavelength of the light is important, but probably more important is the amount of focus. (For instance, visible light isn't very dangerous unless it's focused in a laser).
Product: http://theeyetribe.com/
Here is their quote about safety on the FAQ:

Yes, The Eye Tribe Tracker complies with the essential health and
  safety requirements set by the FCC and CE directives. The Eye Tribe
  Tracker is using near-infrared illumination, it conforms with the EN
  62471 standard and we have obtained an EU declaration of conformity.
  Our hardware has been tested and approved by a certified lab according
  to said standard, and is therefore safe to use.

Related question:
Is it safe to look at infrared LEDs?

Unfortunately, personal medical questions and health advice are off-topic on Biology. We cannot safely answer questions for your specific situation and you should always consult a doctor for medical advice.

I understand. In that case: http://health.stackexchange.com/questions/10396/is-near-infrared-focused-light-safe-for-your-eyes


text:
Question about the consequences of non-random mating and allele frequencies
I just began studying population genetics, and I don't understand something that is written in my lecture:

Consequences of non-random mating:

More homozygote and less heterozygote individuals in the population
Allele frequencies are constant (not in case of negative density dependence)
Genotype frequencies change

What I don't understand is the second point. If the genotypes' frequencies change, shouldn't the frequencies of alleles change as well? Furthermore, I don't really understand either how this is supposed to be linked to a negative density-dependence case...
Any help is welcome! :)

Out of context at least the small piece of text you cite is very poorly phrased and partially wrong.
First, you should have a look at Solving Hardy Weinberg problems. Take your time and read that post... Done? Good.

More homozygote and less heterozygote individuals in the population

This is wrong as non-assortative mating might be disassortative mating where individuals are attracted to individuals of different genotypes.
However, it is true that population structure will cause excess of homozygotes. This is called the Allee effect. The loss of heterozygosity due to population structure is equal to twice the variance in mean allele frequency among those populations. These details sounds a bit too advance for your needs though so I won't go any further.

Allele frequencies are constant (not in case of negative density dependence)
  Genotype frequencies change

Constant over what? Change over what? Not over time necessarily (at least not unless some other assumptions are being made).
I guess what is meant is that if in a given generation mating is not random (due to population structure for example), then you expect the same allele frequency as if it was random but not the same genotype frequency. If it is not clear why, you should probably reread the post "Solving Hardy-Weinberg problems"

Much further discussion in both english and french on @AlissaDeschamps misunderstanding can be found here.

Thanks for your answer! I read all the post about Hardy Weinberg and solved all the problems, but now I still don't understand why the allele frequencies should be constant under non-random mating, and I don't understand either how re-reading the post is supposed to help since Hardy-Weinberg is assuming random mating... I imagined a situation where there would be non-random mating (such as positive assortative mating) and a change in genotype frequencies, but I got a change in allele frequencies as well... So, could you please help me a little bit more? Thanks in advance!

I think your issue has to do with the phrasing (but I am not sure). The allele frequency is the same whether in a given generation mating was random or not. It does not mean that the allele frequency is constant over time. If mating is not random, then the H-W expectation won't hold and genotype frequencies won't be that easy to extrapolate from allele frequencies. But it does not change the allele frequency in any way different than if matin was random (assuming there is no selection at least).

Let me know if that helps and don't hesitate to keep going with further question to narrow down to what is unclear to you.

Thanks a lot for the help, again. However, I'm now more confused than before. If it does not mean that the allele frequency is constant over time, then what does "allele frequencies are constant" mean at all?... (I'm now considering trying to answer the question "what are the consequences of non-random mating" without looking at my lecture, since it became so confusing to me... but if you're ok to help me again, well, it would be welcome and greatly appreciated.)

Totally out of subject, but I just visited your website, looked at your CV and noticed that you studied in Neuchâtel :) That's the city I come from and I'm studying biology in Fribourg... le monde est petit! ;)

Let's continue in chat...


text:
Misunderstanding about nucleotide biosynthesis
Some months ago, I asked what was a phosphoester bond, because I didn't really understand the following picture and explanations provided in the "Molecular biology of the gene" from Watson, Baker, Bell and al. (7th edition).

The explanation is the following:

We can think of how the base is joined to 2'-deoxyribose by imagining the removal of a molecule of water between the hydroxyl on the 1' carbon of the sugar and the base to form a glycosidic bond (Fig. 4-2). The sugar and base alone are called a nucleoside. Likewise, we can imagine linking the phosphate to 2'-deoxyribose by removing a water molecule from between the phosphate and the hydroxyl on the 5' carbon to make a 5' phosphomonoester. Adding a phosphate (or more than one phosphate) to a nucleoside creates a nucleotide.
Thus, by making a glycosidic bond between the base and the sugar, and by making a phosphoester bond between the sugar and the phosphoric acid, we have created a nucleotide.

What I didn't understand months ago was, to resume, "why is the bond between the phosphate group and the 2'-deoxyribose called a phosphoester bond since the phosphoester bond (which is, by definition, a P-O bond) already exists before the bonding between the phosphate group and the sugar?"
While this question is still bothering me (I was not entirely satisfied with the answers I got back then, because the synthesis of a single strand of DNA is something which is probably different from the synthesis of nucleotides themselves), the question I'm asking myself right now is: "why do general biology books always talk about condensation reactions, while this article and this book do not mention it in the biosynthesis pathways of nucleotides?"
What I mean is: it seems like the biosynthesis of nucleotides is far more complicated than just being two condensation reactions. Furthermore, when I look at the 10th step of this picture (which comes from the article I mentioned above), I see a condensation reaction at the end of the pathway, but it does not occur where the book from Watson and al. suggests it should:

So, after months of wondering and researchs about all this, my final question about this is, as mentioned above:
Why do biology books always mention condensation reactions while, apparently, it doesn't have a lot to do with the manner in which the nucleotides are synthesized?

I'm voting to close this question as off-topic because this list is about biology, not the motives of authors of texts, which in any case can only be a matter of speculation.

A condensation reaction is defined on Wikipedia as

a reaction in which two molecules or moieties, often functional
  groups, combine to form a larger molecule, together with the loss of a
  small molecule. Possible small molecules that are lost include water,
  acetic acid, hydrogen chloride, or methanol, but most commonly in
  biological reactions it is water.

It doesn't say anything about the number of steps required to reach the final compound, nor about the type of bonds formed. Following this definition, the nucleotide synthesis occurs via condensation reactions.

Thanks a lot for your answer. However, it still does not explain why the book from Watson and al. talk about the loss of two water molecules, and it doesn't explain either why that same book explains the synthesis of nucleotides in such a simplistic way, while it is apparently way more complicated than just a phosphoester and a glycosidic bond...

It is a simplification but it is correct. You start with 3 molecules, you end up with one via 2 condensation reactions and you lose 2 H2O in total. What is the problem? the schematic is pretty straightforward.

If it is really what happens, then there is no problem anymore. The last thing that is still bothering me is that phosphoester bond thing.