CharonY

I am surprised that the transcription would go down. The question I would have is what the reasons are. For instance, under which promotor is the GFP? Technically, with a very good optical setup (say, confocal) one could detect GFP down to a single molecule, though this is obviously not always possible. However, if there is at least some expression but even IHC does not work, I am also not sure whether FISH would yield much more. FISH in tissue does not have terribly good sensitivity. And RNA Fish is not going to help if transcription is really low. Maybe first check the transcription level (as opposed to only look for the gene?).

Well I cannot say that I share your enthusiasm of Hannity, considering his ehm "liberal" relationship with facts.

Well, here is the thing, as you just realized, the mutation rate is dependent on a lot of factors (also I am currently not aware of studies that showed this correlation, considering that the stability of the environment is not trivial to assess). The dominating ones being the mechanisms of replication rather than the fitness landscape being the dominant one. Note that variability of mutation rate can be triggered on the individual level with stress being the key component. They do not simply select for error prone replication but rather balance it out (i.e. no movement towards higher mutation rate is found on an overall basis). The point is that mutation rates are controlled and balanced out by a large number of factors and mechanisms and may find local maxima at which it is maintained as any increase may have immediate consequences for their fitness. For these reasons the teleological assumption only holds if we oversimplify things and ignore existing data. Look, there are both upper and lower limits for mutation rates, with the lower being the restriction of variability and higher being the rise of deleterious mutations. As you acknowledge yourself the individual history (including the mechanisms involved in controlling mutation rates) is a major determinant these boundaries. This includes to ability to have higher (or lower mutation rate) at any given variability of a given environment. For instance, organisms that have adapted to a given stressor can maintain their fitness without increasing mutation rate. For an organism that is not adapted to it, a higher mutation rate could eventually lead to fitness increase. Again, it is biology. It is usually more complicated than you think. And oversimplifying it often leads to wrong conclusions.

Well, the website is quite full of drivel, but it appears that the lady has been around for quite a while (at least since 2008/9). No doubt that the current election will be used to boost interest. I will have to try to dig some older articles to figure out details, since the newest articles appear to be from partisan websites with reports that are written more like opinion pieces. There is something on wiki, however, under the entry for O'Reilly: And apparently she only started whistleblowing after getting fired. Since a (very) quick search revealed no mainstream media articles (even on Fox, if we disregard the opinion shows) I am somewhat skeptical for now.

Well, this is only partially true. To avoid confusion I would like to state that this is only indirectly linked to mutation rate, however there are quite a number of unicellular eukaryotes with enormous genome sizes. An example is for instance Polychaos dubium with a genome size of more than 200 times that of humans. Size selection is actually somewhat complicated and not solely dependent on replication speed. However, the mutation rate is more related to genetic density rather than size alone (although these are usually correlated).

Well, this does not conform with data. According to this all pathogens or organisms living in changing environments should have mutation rates and this evidently not true. The mutation rate (as expressed per genome) is extremely different if you just compare DNA-based to retroviruses, for instance (several orders of magnitude). Even within a group the rates vary quite a bit (though high-quality data is sometimes lacking). Eukaryotes have higher mutation rates than prokaryotes, but this is because they have basically more area to play around with, before things become detrimental (i.e. the genetic density is lower), despite the fact that many prokaryotes experience vastly different environments even within a single life cycle (e.g. transition from free-living to host-interaction).

Yes, they do. It will depend a lot on location, I presume. According to Moon in his area it appears to be rather frequently and safeguards may be prudent. However, I would think that in most areas the risk is negligible. Why I consider it relevant is that the safety is a big argument for having quick access to guns in your home. This has several implications. The first is that people are afraid. My question is whether the fear is justified (and again, this is going to be area-dependent) or whether it is just a media-inspired fear. I.e. whether the actions taken are in no relation to the actual risk. Examples for bad risk assessments would be e.g. having a gun in the house, but no fire extinguisher. Or a gun in the car, but not wearing seat belts. It is kind of odd, but living in the US has made me realize that fear is quite pervasive in society and in many cases it does not really correlate with real risk. Of course things happen, and it may happen to you or someone you love and in retrospect you would have wished that you have prepared accordingly. However, everything is a matter of chance and people choose very strange priorities, and I think that people are being manipulated by it. Guns and the safety argument appear to be a very strong factor. In other countries where guns are allowed the relationship appears to be quite different.

That is unfortunately true. Many of these rules are extrapolations limited association studies. Hardly anything is based on mechanistic knowledge, for example. There is simply a huge knowledge gap regarding the interaction of the genomic background of an individual, diet, and health outcome. For the most part it seems that one can give general guide lines, as well as certain reasonable set of rules for specific conditions, but other than that there is a lot of guess work. Some are doing a better job by actually taking metrics (other than just weight) while applying certain diets, but there are far too few of these around.

Ohhhh please do. Ouch, that hurt.

Just out of interest, are there statistics regarding home invasions? Unfortunately it is not a listed as a separate crime but rather falls into e.g. robbery or assault. But I am interested in figuring out how high the risk is in relation to e.g. accidents (touching on something that was said earlier).

Note that parasitism does not refer to pathogenicity. Initially it was based mostly on a trophic relationship, i.e. exploiting the host as a source of nourishment (and usually as habitat), whilst providing no nutrients in exchange. Since then it has been used in different contexts under slightly different definitions. However, from a classic point of view viruses are therefore not parasites (regardlesss whether pathogenic or not). From a molecular biological point of view one could define mobile genetic elements as parasites (of the genome) using non-classical definitions (as it is occasionally done) but most microbiologists would not like that too much.

For injuries cold is obviously the preferred option, for the reasons highlighted above. I.e. inflammation should usually be treated with cold. However, chronic pain can also be caused by inflammation.

If it was, it is quite a mess of questions. It kind of garbles up a number of terms, IMO.

Not like that. There are too many uncertainties (i.e. environmental factors) that would be impossible to predict population-wide changes. The only possibility would be under highly controlled conditions (the Lenski experiment would be an example). I was given the example of function prediction based on the protein sequence. I think the basics should be covered in quite some textbooks. Check this out, for example http://www.ncbi.nlm.nih.gov/books/NBK21086/. Without evolution as a basis the whole approach would be non-sensical.

Of course biology has models or predictive power. In many cases they tend to be more qualitative in nature, however. You may want to look up how e.g. genome annotations are conducted, just to get an idea on this topic.

I think we are in different incompatibility groups.

I feel you may still be missing the point. Let us say, we want to sequence an organism. First of all, we would assume that DNA is the carrier of genetic information. Why? Because evolution. Then, if we sequence it, we use methods that differentiate the four bases. Why? Because evolution. The way we then detect open reading frames, deduce protein coding sequences, identify the amino acid sequence thereof and predict functions are all possible under the theoretical framework of evolutionary theories. Without them the approach would have to be radically different. It is therefore not only selector of bullshit (which it sometimes is, but probably not that often in a scientific context) but it is really the foundation of many actual approaches.

The point is that while you are still learning the basics, it is very unlikely that you will come up with any relevant or novel ideas. As others have said, you have to know the current knowledge on a given subject (which takes quite a while to master) and then you can develop new ones. Many ideas that you will have now, will appear foolish to you, once you have studied them further. One of the first prerequisites of learning is humility. One has to acknowledge that the knowledge one currently has is insufficient. Only then does one open ones mind to learning. Incidentally, much of the college time will be spent realizing how little we know in various fields. Much what we have learned from textbooks in high school are just extreme simplifications to make the topics more digestible. The desire to try to understand even a tiny little bit more is what drives scientists. But first one has to have a (somewhat) clear vision what is known and what not.

It is actually slightly more complicated. Bottom line is (as correctly pointed out) cold restricts blood flow, numbs pain and reduces inflammation. Heat promotes flow. The question is therefore less whether the pain is acute or chronic, but rather what the mechanism behind it is. For most acute injuries pain numbing and reduction of inflammation is beneficial. However, even with chronic pain cold can be advantageous if the source is inflammation. However, heat can promote injury healing (by increasing blood flow)...

Ann interesting article describing how young gorillas learned to spot and dismantle traps. http://news.nationalgeographic.com/news/2012/07/120719-young-gorillas-juvenile-traps-snares-rwanda-science-fossey/?source=hp_dl2_news_smart_gorillas20120720

This is not my field, but do you have an specific questions in mind?

I am quite confused. In the provided link the author (Dean Baker) is actually saying that Krauthammer is just giving "the right-wing caricature of the left". And then continues stating that I wonder whether you agree with Krauthammer or Baker here. Krauthammer's post is mostly a drivel attacking Obama using repetitions of well-known talking points starting with misquoting Obama. "Caricature" is actually quite fitting. So, a lot of opinion there, but little theory.

If you are lazy and have access, solid phase extraction columns with C18 can also be used. Or pack them yourself (though arguably doing LLE is easier at that point).

Bloody hell. And pretty good posts on top of that. Also it made me realize how many fans he got. Why are physicists always the popular ones? And how does he keep up with his work? I have to steal his delicious brain. Hmm, brains.

This is rather an oversimplification and a comparison that does not hold much water. First of all a virus is generally considered a mobile genetic element rather than an organism. Second of all, infections have in common that they need to find a compatible host, circumvent immune responses and possibly deal with competition in their particular niche. Now here is the point were strong or weak is something that is not really useful in the discussion of diseases. First of all, quite a few of the symptoms involved in disease response, including some rather harmful ones, are not due to the primary actions of the pathogen, but are triggered by the immune system. The cytokine storm is the textbook example for this. In this case a strong immune system (in terms of giving strong immunoanswers) becomes a liability. Second, most pathogens do not actively try to hunt down their prey. In fact letting them survive is quite an efficient tactic, too (just look at all the viral DNA in our genome). Especially in viruses a longer co-evolution between host and pathogen results in lower virulence.