CharonY

I think Marat put the facts quite into a wrong context. The main criticism on the US health system is less that it is awful and everyone is dying left and right, but rather that it is more expensive than other developed nations, without providing a better outcome. Regarding education it is probably more that the US was losing a lot of ground on several areas while (I believe) it used to be in the top spot. The difference between self-assessment and actual results may also play a role. According to the OECD survey 2009 USA ranked 30 in mathematics, 23rd in sciences (slight improvement compared to the last, I believe) and 17th in reading (the focus of the last survey).

Are the differences significant? Well, they are, though I do not have the values with me right now. What I do have is a statistical test of the countries as difference of the OECD average of each tested element (e.g. reading comprehension). Based on that, the US is roughly OECD-average (not absolutely abysmal) in most areas, except mathematics, where it is significantly below the average.

Regarding poverty, I recall someone mentioning that the heritage foundation article was not really reliable for some reasons, but I have to ask (or read up) to figure what it was. Though glancing to the list this

The average American "poor" person has greater living space than the average person in Paris, London, Vienna, Athens, and many other European cities. (The average citizen there, not the average "poor" citizen.)

There will not be a terrible amount of trouble, but quite a bit of additional paperwork. Essentially you have to demonstrate that what you do is worthwhile, that no viable alternatives exist and that relevant procedures are taken to minimize pain and distress. Normal requirements, especially for NIH funded projects, also include training in that area. Essentially the requirements for the respective animal welfare laws have to be fulfilled (as well as certain other guidelines). These apply to all vertebrates.

The ethics committee mostly works with you to fulfill these requirements.

Could you provide the reference and abstract, please?

It would costs far more than a few thousand to accomplish. You would have to first make a transfection construct (i.e. a vector containing GFP or GFP fusion with correct promoters) then transfect and then select for those with successful transfection. Essentially you have to create a mutant that actively expresses GFP (or luciferase for luminescence). While the construction of the vector is relatively trivial (but requires somewhat costly equipment to function efficiently). The actually transfection (i.e. insertion of the vector and hoping for efficient recombination) is a rare event, meaning that you have to screen a lot until you find a cell that got it. Definitely not a very good DIY project.

Well, quite a few vitamins are lipohilic and do not get secreted efficiently. These generally carry the highest risk for overdosing, as they may accumulate to some extent. In many cases and on normal diets many supplements have little beneficial effects. In contrast to what Marat claims, there is little evidence that high doses have wide-ranging beneficial effects (conspiracies aside).

Iron is one of those from which many women actually do benefit, though, especially on diet with low iron content. The toxicity is, for the most part low, though one should be careful e.g. in cases of infections or intestine problems, as high levels of available iron can allow bacteria to grow more efficiently. This also goes for pathogenic ones.

Also note that adverse effect levels are usually rough estimates. One should try not to use those levels as hard safety limits.

There are a number of finer biochemical characterizations in which binding and subsequent transport (though the latter can essentially only be shown indirectly). Check the annual review:

Kaplan

BIOCHEMISTRY OF NA,K-ATPASEAnnual Review of Biochemistry Vol. 71: 511-535 (Volume publication date July 2002)

The basic difference is how they are derived. Breeds are, well, bred. Strains usually have smaller defined genomic differences. Note that there is an overlap, as defined strains could be derived from breeding. However, all individuals within a strain are genetically uniform.

Eh, for a research position it is really risky, unless you are well connected. There are not that many research positions available. Truth is that most lab research is done by grad students or postdocs. And the letter only for a limited time (I have seen quite a few engineers without postdocs). Other than that in many jobs you would be more group/ lab leader (i.e. being removed from research) but these positions are usually very competitive. There are also industrial R&D positions, though but apparently the job pool is kind of limited, at least in areas I am familiar with. If you are well connected, it may be worth a try, or at least ask around to look, what kind of positions are really available. Otherwise you may be set yourself to be overqualified for the job you got right now and not be competitive enough compared to the fresh 20-something PhDs (unless your current job gives you some kind of edge, however the edge may be considered dulled after a PhD hiatus).

This is not even the real issue here. AFAIK there was progress in creating tissue from stem cells, but not yet fully functioning organs. Also, getting fully functioning stem cells is non-trivial to begin with. Reversing adult cells to become pluripotent again requires regulatory manipulations which enhances tumorigenesis (as the normal regulation leading to differentiation has to be knocked out). This is very unlikely to be beneficial right now.

Two mechanisms. First is its antibacterial activity, mostly due to the generation of oxidative stress. Second is chemisorption and catalytic removal (the more relevant part here).

Both have to be balanced out. As the exchange is by diffusion a proper gradient for both gases (in opposite directions) have to be maintained. Impeding CO2 transfer would lead to hypercapnia.

People are over-reacting...the scientists aren't even sure how Arsenic is incorporated into it...

Well that is not a particular mystery for the most part. The basic asumption is that due to the equilibrium shift P would subsequently be replaced by As. Normally, this would result in inactive biomolecules and eventually death of the organism.

In many ways gametes are not much different than other highly differentiated cells. Certain signals resulted in the activation of regulatory pathways that eventually led to the formation to their current state (i.e. gamete) and everything that is related to it (including no substantial cell growth etc.). This is true for about any cell type you find.

Essentially regulation is the key. This is even the case in unicellular organisms that do not differentiate. Up on certain cues (could be anything starting from nutrient availability, stress or quorum sensing), certain regulatory networks activate/deactivate leading to very different cellular responses, despite having the same genome.

Yeah, that makes sense, Ringer, but whatever is picked up by the retina does get sent to the brain, does it not?

Absolutely not. There is heavy modulation and editing going on before the signal reaches the brain. The way it works is not that there is a specialized cell that can spot a pattern per se (how is it supposed to do it, it only gets a signal and then transfers it). The trick is than the signal reaches an ensemble of cells that are connected in such a way that they cumulative respond to a specific stimulus.

In simplified form, imagine a row of cells. The right cells inhibit the cells to their left, whereas the left cells induce the ones right of them. What happens is that if a light source moves from left to the right, the net signal is a very strong one, as the first cell (outermost left) gives out a signal and then increases the output of the neighboring cell when the light reaches it.

On the other hand the same cells are non-responsive to movements from right to left. Thus you have a group of cells that are specialized to left-to-right movements.

Note that this kind of modulation is, with exceptions, not necessarily located on the retina itself, but also in cells on the way to the brain.

Specialized effects as e.g. cells specialized in detecting contrasts or specific patterns and movements are wired like this. The brain only gets a heavily edited version of what is going on in the retina.

I would say that unopened cola would be virtually sterile. During the manufacturing process there is little which promotes growth, and the things in there, like the pH (phosphoric acid) and high sugar content (close to 200 mM based on rough calculations) would be stressful to most cells. Opening it up would be a different thing, though. Still, osmotic and acidic stress for most, and I am not sure whether there may be additional nasties in it.

That's easy to say in hindsight. But I suspect that if someone asserted the presence of significant amounts of noncoding DNA BEFORE it was discovered, the mainstream evolutionists would have dismissed the idea. "Why would there be noncoding DNA? It would just get in the way. And besides, where would it come from? "

 

IF it is "what physiologically is expected" why did no one expect it? If you have a reference to someone predicting the discovery of large amounts of noncoding DNA, I'd like to see it.

Dude, you are still operating under the wrong assumption what junk DNA is. It was very well known that gene expression is dependent on stimuli and is necessary for cell differentiation. Just following logic, how the heck are cells supposed to differentiate when there are no expression differences. Also, gene expression analyses have been done for ages. This would be quite futile if there were no differences to be expected, no?

Also non-coding DNA with regulatory functions are VERY well known. How, do you think, is transcription regulated (textbooks may help you here). A surprise were the detection of functional sRNAs (they were simply not known as class and have not been detected).

Seriously, read a basic genetics textbook and then we can discuss some more. I see little value in discussing erroneous assumptions.

I assume that the transferable diseases were mostly parasites (as ewmon mentioned) as well as a number of viruses. Bacteria tend to be somewhat less specific in that regard.

It is hard to tell from the description, but the failure of DAPI is suspicious. First, are you sure the microscope is working? I.e. even without stain you can see your cells well in transmittance light? And second, the cells are Ok?

Knockdowns are very useful.

Actually evolution does not consider individuals per se (selfish genes are mostly interesting in terms of specific mechanisms), but always focuses on the population. The key is allele frequency. They are, by definition a description of the state of the population. There is no individual resolution. From that standpoint individual changes are almost always relatively inconsequential, with few exception. This may include extremely low population sizes, or enormous selective pressures, which would rapidly increase the frequency of the involved allele(s).

Again, evolution is all about population changes. Not about individuals.

Actually, certain teleological elements in the broadest sense are somewhat possible. For instance, loss of certain functions may lock the future direction of a species (if the re-occurence of the mechanism by whatever means is highly unlikely), especially assuming an otherwise constant environment. Under these conditions (and probably some more that I did not think of right now, like e.g. the proportion of fixed alleles in the gene pool and whatnot), the possible directions of evolution may be limited to such a point that a certain endpoint appears inevitable.

Though I probably would not call it teleology in the classical concept (i.e. final cause) as it is more the consequence of certain mechanisms (or lack thereof). It would be a bit akin to invoke teleology to explain gravity, for instance.

Regarding non-expressed genes. This is what physiologically is expected from about every cell. Not even in prokaryotes can anyone expect to see every gene to be active. They are regulated by internal or external stimuli.

The basic premises in the OP are simply wrong.

Actually I remember that at least in many of the more famous battles the mongols were numerically inferior and were victorious due to superior tactics. They excelled in the use of flanking tactics, though. Eventually this could result in encirclement.

Perhaps the error is yours. You seem to have misread the context of the OP's illustration. the first paragraph referred to what is traditionaly called "junk DNA" the second paragraph described silent genes in particular cells. The third paragraph suggested that one possibility is that "Junk DNA" may be in a sense similar to silent genes in that this junk is actively conserved feed-stock for future needs. I welcome the OP's elaboration if I have this wrong.

Not as the OP describes it. Here:

Each cell type looks and acts differently from the others. But, because they all inherit the same genes, there must be a lot of junk DNA in each type of cell. Brain cells don't need genes that function uniquely in liver cells, nor do kidney cells need genes that function uniquely in skin cells.

Junk DNA is clearly referred to genes that have no function in a specific cell type (as opposed to another). Also note, while there are genes that are not expressed anymore in certain tissues, they may have very well been active during differentiation.

Also this is not quite accurate

What aspect of evolution theory predicts that long stretches of inactive DNA would coast along inside organisms, seemingly contributing nothing to their survivability? Nobody saw it coming. It was an empirical surprise.

It would only be surprising if the additional DNA came at a cost with no benefit. This appears to be somewhat true in e.g. prokaryotic and, even more pronounced, in viral genomes, where DNA size places a considerable cost on the organism. However, in eurkayotes genome size is much less limiting. So even in absence of benefits an increase would be considered neutral or near-neutral. Viral resilience have been put forth relatively early to explain an expansion of genome sizes in eukaryotes and, as mentioned, quite a bit of the junk DNA can actually be assigned to regulatory or structural functions. Once the cost restraint of DNA was lifted in higher eukaryotes expansion of genome size could lead to benefits that overcome the (in eukaryotes) relatively low additional cost for DNA synthesis.

If they gave me some samples I could run it through the MS for a few bucks.

Don't have much time but there are a number of factual errors in the OP:

But in the context of ontogeny, the development of organisms, it is exactly what is to be expected. Each cell in the body of a complex organism inherits the same genes from the ancestral zygote, the original fertilized ovum. Despite all possessing the same genes, brain, liver, kidney, and skin cells, for example, distinguish themselves phenotypically. Each cell type looks and acts differently from the others. But, because they all inherit the same genes, there must be a lot of junk DNA in each type of cell. Brain cells don't need genes that function uniquely in liver cells, nor do kidney cells need genes that function uniquely in skin cells. But all the cells inherit all those genes from their common ancestor, the zygote, whether they need them or not.

This is not what junk DNA is. Essentially they refer to non-coding regions (though with the discovery of sRNA this has to be expanded somewhat). Genes that are silent (in a given tissue) are not junk DNA.