CharonY

Well, unless you cultivate anerobically you will always have a slight exchange of your flask with the surrounding air, which is sufficent for phage infection, for instance. But then you would see lysis after inoculation with infected cultures. Odd indeed. So if I understand you correctly you only have trouble when inoculating from liquid, but not if directly from plate (as your o/n cultures)? This would also speak against phage infection in the incubator as these cultures should be equally affected. Have you tried new pipets?

Atheist, thanks for the correction. I just looked up Cologne. It has ~900k. Read that Frankfurt is the fifth largest German city, though. Well looked bigger from the plane, whereas Munich appeared to be slightly, well, more rural.

That is odd. If there is really a phage infection (and sudden lysis of colis usually indicates that). Though I wonder, do you inoculate massively? I mean if you inoculate with a single colony you would not observe lysis within two hours, would you? So do they simply don't grow or does it really clear up? Does this lysis only occur in liquid medium (standard LB?)? That, is you don't have lysis on your plates at all? Have you tried to mix inoculated, grown E. coli cells with lysed cultures? Phage contamination is a rather serious matter, though.

Uhm, were did you pick that up? I mean some have greenhouses, but more have gardens or nothing in that regard. Modern houses are usually firmly insulated to avoid heat loss, though (energy conversation appears to be a rather big issue). And as Ecoli said in the US are strong aggregations in some urban centres as are in Japan. In Germany this tends to be less the case. At least I think that the there are not that many giant cities as in the US or Japan. Actually I think Berlin and maybe Frankfurt are the only ones that might qualify (and still being dwarfed by, say New York or Tokyo). On the other hand if I recall correctly the standard of living and especially healthcare is one of the highest in Japan...

In that case I wonder why there was not a simple demonstration without dropping it on two(!) cities. The Japanese were already negotiating peace conditions (actually afaik they were opposed to removal of the emperor while the USA demanded unconditional surrender, but maybe there was more to it). And if it was also intended as a demonstration of power against the soviets, they could have been invited too...

I just came across a paper describing the evolution of Pseudomonas aeruginosa, an opportunistic pathogen that is often found in lungs of cystic fibrosis patients, into a less virulent pathogen within eight years. This is quite an intersting observation of recent (co)-evolution. Here is the abstract: In many human infections, hosts and pathogens coexist for years or decades. Important examples include HIV, herpes viruses, tuberculosis, leprosy, and malaria. With the exception of intensively studied viral infections such as HIV/AIDs, little is known about the extent to which the clonal expansion that occurs during long-term infection by pathogens involves important genetic adaptations. We report here a detailed, whole-genome analysis of one such infection, that of a cystic fibrosis (CF) patient by the opportunistic bacterial pathogen Pseudomonas aeruginosa. The bacteria underwent numerous genetic adaptations during 8 years of infection, as evidenced by a positive-selection signal across the genome and an overwhelming signal in specific genes, several of which are mutated during the course of most CF infections. Of particular interest is our finding that virulence factors that are required for the initiation of acute infections are often selected against during chronic infections. It is apparent that the genotypes of the P. aeruginosa strains present in advanced CF infections differ systematically from those of "wild-type" P. aeruginosa and that these differences may offer new opportunities for treatment of this chronic disease. Smith et al, Proc Natl Acad Sci U S A 2006

Go to either ncbi or even better, the swissprot database, and search for the proteins. It would be even better if you knew from which organism they were isolated from (although the difference would not be very large in any case). Different organims could easily account for slightly different numbers in the MW that you may have found.

Actually if you already have homologous sequences (as your approach suggests) then you could simply align those sequences and look for conserved regions, make primers against them, blast those primers against databases to check if they are specific for this gene and try to amplify it. If you want to see if it is expressed a simple RT-PCR should suffice.

After reading the original thread from which this statement came from I have to retract my above post. My bad. I might disagree with the statement per se, but if stated as his own (or a general) opinion it is of course perfectly acceptable.

Actually I think you are thinking a little bit too complicated here, sciop. This is probably only a exam question. Since it is stated that it is a lacZ negative E. coli, one can assume that the mutation is in the lacZ gene (otherwise this info had no meaning). Now the mutation that is sought will be a combination of the UV (dimer formation) and polV (sloppy replication across the resultion lesions). PolV is known to be able to bypass stalled replication forks but it has a low fidelity. Furthermore it is known that PolV not only bypasses for instance TT-dimers with high efficiency but also tends to incorporate a guanine opposite the 3'-thymine of a TT-dimer. I think the rest should be obvious.

I agree with the first three posts. And furthermore quite a number of "irreducible" complexity examples have been in fact been debunked. As such the first sentence already is a very weak statement to begin with. Edit: wrote whlily YT2095 posted Actually while reflecting about it I think I have more quarrels with the vagueness of that sentence. The "can" for instance. The hypothesis should be something in the line of which structures are too complex to be derived from evolution. But as I said, some complex structures have already been resolved. As such I'd object to such a general statement.

What you describe is basically tied to whole brain areas, not individual neurons. The brain consists basically of two hemispheres (left and right) which control (and get information) from the opposite body part. So roughly your left body parts are controlled by the right brain hemisphere and vice versa (there are small cross-overs, e.g. in the visual pathway, but I will neglect it here). Generally all the signals are integrated by means of the corpus callosum, which is a broad band connecting both hemispheres. Now the persons you describe typically have a severed corpus callosum, meaning that each brain hemisphere can only work with the data it receives and cannot exchange information with the other half. So if such a so-called brain-split patient sees something with his left eye (sending information to the visual area in the right hemisphere) he will only be able to point at it with his left hand (also controlled by the right hemisphere). The other half of the brain is totally unaware of it.

Bascule, you are of course correct. What I meant with repetition is a tautaology as a stylistic device rather than in the context of logical statements. I should have been more preciese. Dak, the statement is true, but tautologies are invalid as a logical argument. Basically in the same way that circular arguments are.

Essentially there is no real conflict between gradualists and punctualists (as in fact the dissent was rather smaller than it appeared to the public to begin with) any more. It is clear that evolutionary rates can and do vary. The real question is whether apparently faster evolution in terms of geological time scales can be interpreted as an absence of microevolutionary modifications (based on estimates of reproductive time scales). That is if there are macroevolutionary events that are not linked to microevolutionary ones. The evidence is quite lacking though, therefore the general consesus (as far as I am aware of) is that it is still explainable by microevolutionary models.

Tautologies are in general some kind of truisms or repetitions that possess some kind of redundancy and hence do not add information. A tautological logical statemen is for instance: "all swans are white or not." This statement will always be true making this an empty statement. In everyday language tautologies can be empty repetitions like e.g."Salsa sauce" or "HTML-language." In most cases it is considered a bad style because you essentially do not add any information but only repeat yourself by stating the same (this is another one btw).

There is no significant difference in xxx contamination between rural and city environments. While it is not my field of expertise I am a little bit doubtful regarding nitrate and possibly iron contamination between rural and city areas, btw. I am not sure if for instance fertilizers in rural areas might not raise the contamination to city levels. And regarding iron, especially in anoxic subsurfaces and aquifers the concentration can be extremely high. Just some random thoughts, though.

Actually only few organisms maintain a certain temperature and furthermore, the question was (at least as I understand it) if they could actually convert it to energy. And here the answer is quite obvious, as electron transport is clearly involved in energy (ATP) production, whereas heat is not. Sorry, while I am not a big fan of making multiple choice tests (but they are sooo much more time efficient). I actually fail to see that they are badly constructed (with the caveats Atheist gave).

*Alaps snail on the head-hard* Ahh. I needed that.

With my full name I only get my papers. Suppose no one is really that silly to give a kid that kinda name Except, obviously, my parents.

In the simplest case there are two pools on which selection can work on. First are mutations that only exist but have not yet been subjected to selective sweeps (that is, they are already spread in the population but are dormant as stated above) or they are new traits or alleles that are not fixed yet. In the latter case (and that is probably what gmacrider is thinking of) the frequency of the new trait being fixed in the population (that is not being directly eliminated after selective sweeps) is a function of the frequency of its occurence and its effect on the fitness of its carrier. If the increase of fitness is vast, only few occurences (or as proposed above, possibly one single mutation) might be needed in the population before it gets fixed and may start to spread. But this is a rather rare case. In most cases the effects beneficial effects are very low. As such most models would require at least a moderate frequency of occurence of a particular mutation to allow it become a fixed element of the gene pool.

The definition of transient species is a bit fuzzy. For instance, all now existing organisms can actually be seen as transient form between neighboring taxa. But just to add some to transient fossils, there are quite a lot of examples around. Not only hominids, but also foraminifera or the famous transition from fish to tetrapods. As such the given claim that no transitional fossils have been found is ridiculous at best.

I am aware that the question was not directed at me, but actually you could answer the question by yourself by careful reading. The varying replicators are essentially the genes (read a lil' bit about the selfish gene theory to understand why Dawkins is talking about genes as the replicating units and not the ). Genes vary randomly (as mutations usually do not follow a predictable pattern, resulting in different alleles), but there is a non-random selection against detrimental alleles. That is, those that survive improve the fitness of their carriers, or are at least not detrimental. This is a selective process and hence, non-random.

Basically the mechanisms of evolution (mutation, genetic drifts etc.) are random, but selection shapes it. Those that survive are those that under the given selective force have a higher fitness. Therefore this process is not random. Of course, if you take a global historical view one could argue that the changes of selective forces do not follow a distinct pattern and thus the whole process is random.

Well I suppose it can be argued that a Liger is not a species as tigers and lions are allopatric species. As far as I know that do not have a species name assigned because they of course do not exist in natural habitats. So in theory they do have an isolation of gene pools. But in general I do agree. Species concepts are not clear cut functions and especially with regards to protists and especially bacteria more a matter of agreement. With regards to hybridization, if its effects were significant I would argue that with time the gene pools should eventually merge. This is outside of my expertise but to my knowledge there were no reported instance of large-scale mergers of sympatric populations. With regards to bacteria, this would probably make sense if we got a more thorough view on ecotypes. But our knowledge to bacterial diversity is atm rather sketchy at best.

Actually it is more reasonable to assume that there was no new development of the described immunities, but that they already existed (e.g. due to mutations) and only now they are selected for. It is likely that the given immunity trait was already in the gene pool but only in presence of the disease do we see a phenotype. In other words, introducing a disease will not lead to a new development of resistance, but will only select agaisnt those, who did not already have it.