CharonY

Apparently the Texas GOP is not quite certain about its own agenda: Mind you, that was after all the media coverage of it.

The easiest bridge (in terms of how problems are approached) is probably bottom-up. That would lead from biochemistry to molecular biology. The problem is that the truly "omics" based thinking is (should) be highly physiology dependent, which requires deeper knowledge of cellular physiology and generally a deeper insights about the interconnections at a higher level. Conceptually that tends to be a bit of a rift between chem and bio. That being said, being an undergrad gives you more than enough to look into molecular biology and cell biology. The latter tends to be a bit boring at the beginning as it only starts to shine after you are past the fundamentals (though this is probably true for most things). What I really would recommend is picking up books with these topics and see if it is really interesting to you.

Who is John Galt.

Also, the death of manufacturers of tabletop game miniatures (well, that is obviously a copyright infringement issue, but these bastards have already eaten so much of my money that I feel compelled to single them out).

Well, at least some Iranian scientists were killed. But they are the outliers, if you will...

AFAIK you can basically get everything for building a gun legally, except for the receiver part. I do not know how hard (or easy) to manufacture one of those. 3D printers could make it easier, though currently the polymer material could makes tricky if you do not know how to properly make adjustments. I was also wondering whether it is possible to utilize elements e.g. from replicas together with parts that can also be legally acquired to rebuild a functioning weapon.

I have completely lost the plot by now.

You know, I always wondered whether Swansont's posts were really so good, or whether his avatar made me believe that. Everything with Sean Connery on it appears to be classier. So for science I taped down the right side of my screen and re-read some posts. Still bloody good, darn it. But I need a larger sample size. So I am applying for an R21 with the purpose the elucidate the interdependence of post quality and avatars. I see no reason why it should net get funded.

Actually listening to the whole clip I was under the impression that he was referring to the infrastructure: " If you were successful, somebody along the line gave you some help. There was a great teacher somewhere in your life — Somebody invested in roads and bridges. If you’ve got a business — you didn’t build that." Otherwise the sentence before would be kind of odd. At least to me it looks more like a grammatical error (i.e. he should have said "you did not build those"). It is also revealing that in the attack posts the sentence was conveniently cut out...

I have not read the posted websites, but I am at least partially familiar with the group(s) involved in calling for a new synthesis (I do not know anything about Gert Korthof, though). The biggest issue is still how to integrate the different kind of information we have into coherent model. I share much with Koonin's view due to the work with prokaryotic systems and the fact that the modern synthesis does not apply well to them. Among the reasons is the high rate of horizontal gene transfer (that is quite a bit of a problem to integrate in basically all models) as well as the problems applying a species concept to prokaryotes. The point is that the modern synthesis simply does not account for the molecular data (including functions as well as sequence information). A part that is mostly accepted (again, driven by molecular information) is the neutral theory of evolution, rather than a strongly Darwinian one (in which positive selection dominates). The problem is that many of these issues are in a certain sense subtle that one would not easily notice unless one actually works in the area (or in my case, spend coffee breaks with colleagues that do). As such it is too easy to sensationalize it.

If you claim there is teleology in evolution and claim that variability of the fitness landscape shapes then it must be the dominant one otherwise there won't be a goal within evolution. If other factors are stronger in determining the selective factors, it can easily move towards a different direction (and then it is no different from other traits). As the data shows, an organism living in a very varied environment can have a lower mutation rate than an organism living in a more static one and organisms in the same niche can have very different ones (i.e. just look up a couple on papers, including from Sanjuan's group on viruses, for example). The rate for DNA viruses is about 10e-8 to 10e-6 for DNA (also roughly the rate for prokaryotes, higher ones for eukaryotes) and about 10e-6 to 10e-4 for RNA viruses. The environment in which viruses exist is very similar, so according to the claim you made, their mutation rates should converge. Instead, as I have repeatedly stated, other factors, including genome size are shaping the mutation rate. In other words, mutation rates have, as basically all other traits, an optimum. Then the teleological argument would be that the fitness of an organism moves towards a maximum for a particular trait set (including polymerase fidelity), which is true but not quite the global goal that a teleological argument would aim for, or is it? My main point is that mutation rate is just a trait like every other (with e.g. changing environments being a selective pressure). It is interesting to note that in a PloS paper a few years ago (also from Sanjuan's group, I believe) they found in simulations that mutation rate stay below the optimum in a rugged landscape (I would have to dig it up again for their methodology). Now is that the main point of your argument? In that case you may want to clearly define what you mean with teleology in evolution and how the example on mutation rate is different from the optimization of fitness of other traits? In a telelogical argument I would expect a certain endpoint. There is obviously there is an upper limit in which higher mutation rates clearly demonstrate detrimental effects in RNA viruses (Crotti et al. 2004 PNAS) and this rate is determined by factors such as genome size. As such, I do not see how mutation rates makes a stronger teleological point. With regards to data, I was referring to the actual mutation rates found in viruses and their variability, despite similar environmental conditions and lifestyles. So how is your data coming along (aside from generalized statements)? Right, you just omitted them and claimed that environmental variability will move towards higher mutation rates. If other factors limit it, it will obviously not. So there is no endpoint, really aside from an optimum value. And we are right now at the beginning of the argument again. Where is the frigging endpoint? And how is it different from other traits? That is actually true, I was thinking in terms of the interactions of fitness and mutation landscape and I totally garbled it up. My apologies. Thank you very much for your insights. While I tend to shoot from the hip with my posts at least I usually do not take the extra time to be insulting. How about defining teleology in evolution, add at least some references (considering that it was your claim to begin with) and demonstrate that your post was much more thoughtful than what I spew out?

Actually I am not aware of any kind of uniqueness of human DNA compared to other animals, for instance. The major issues in the use of DNA information is much in terms how that information in conjunction with the cellular content, result in physiological effects and reactions. DNA alone is just a molecule with a certain variation in its base composition.

Hmm according to helmet websites they appears that helmets are certified according to head acceleration upon non-ballistic impact. 200 Gs appears to be the generally accepted. It appears that they are dropped from a given height. I have not found the standardized test info after a quick search, though (must be listed somewhere). But that is unlikely to be easily translatable as the impact area of a bullet is quite different.

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.