CharonY

In addition to that, one should realize that even findings into which a lot of effort has been put in, may eventually be proven wrong or inaccurate. The conclusion should then be that even more effort is required. For some reasons some come to the conclusion that they need less.

The description of the bacterial cell hull composition is slightly confusing. In short, starting from the inside all bacteria have a cytoplasma membrane. This is followed by a peptidoglycan layer. The main difference at this point is that in Gram+ bacteria the peptidoglycan layer is much thicker. In both cases the sugar is made up from N-acetylglucosamine and N-acetylmuramic acid (linked to a short peptide), but in case of Gram+ more elements can be found within the thick layer, including S-layer on top and modified with glycopolymers throughout (which can quite diverse, depending on strain). Gram- cells have an additional outer membrane just past their thin peptidoglycan layer. Capsules are common, but not found in all bacteria and are often formed depending on growth conditions. With regards to the morphologies, these are generally not used as species classification anymore. They are generally only used for rough classification with additional biochemical information available. I congratulate your interest in this field and encourage you to get books on the subject as most websites are going to be awfully shallow and are unlikely to hold your interest for long. Or provide more comprehensive knowledge that is likely to provide deeper insights (eventually).

It is generally not what most biologists would agree on. I am not an expert in this area, but I have the impression that this is pretty much a thing established Cavalier-Smith (though correct me, if I am wrong). Nonetheless, the evidence is not fundamentally conclusive though to my understanding the current weight of evidence is not favoring this view. But then, my knowledge in this area is certainly not cutting-edge and maybe Arete could weigh in on it. What I do is usually let an evolutionary biologist that I trust deal with the changing evidence (and whatever biomolecule is currently en vogue) and let him/her give me a summary so that I do not need to track this issue (or the the different feuds that may be there).

Also it should be noted that even if lab strains are used for bioremediation they tend not to compete very successfully indigenous bacteria. Therefore they often have to be used in large amounts and even then after a relatively short time they tend to be outcompeted by whatever is already present. The reason is obvious, bioremediation strains are used because of their ability to utilize certain toxins. However, in contrast to indigenous bacteria, they have not been selected for survival under the given conditions.

How is that worse than being on a planet without atmosphere or unsuitable for human life? Remember the premise is that we should go and terraform something, which implies that the target planet is inhospitable to begin with. So in order to go there you would have precisely the same problems plus you have the issue of the material to terraform there. It would only make sense if there was perfectly habitable planet to begin with (except logistics would still be an issue). And again, if you have the science to terraform a planet (which is sci-fi at this point), the question is why similar technology cannot be applied to Earth (other than it does not deliver a nice plot device to seek out other planets). Of course terraforming is still not possible and I guess there is relatively little in terms of hard science that we could rely on as empirical basis. Nonetheless, so far I have not seen a good argument why dealing with toxins and pollution on Earth is harder than doing the same off-planet.

I am not sure where the confusion is, but essentially it means that photosynthesis never existed because the organisms capable of it never developed (which is basically just a rephrasing so I am not certain whether that clears up anything).

From a logistic point of view I still fail to see how it is easier to have a significant amount of people survive either in space or even on a remote planet (unless they are, for some weird reason, perfectly suitable for human life) rather than find a corner on Earth and make that inhabitable until the rest clears out. The basic assumption is that e.g. massive amounts of killing would affect every corner of the world. But what about the parts that are not inhabited, say, the ocean, or large parts of the arctic. Or even Canada for that part . Even if there was significant pollution and heavy toxin contamination, how much worse is that from being in space or on a completely hostile planet? In all cases you would isolate the population from the environment.

I do not mean to specifically aim at the above post, but In a way I find it funny that some people have a rather bleak outlook about the future on Earth. However, at the same time they are rather optimistic that these problems vanish or are easily overcome when transferred to another planet. I.e. for some reasons solving problems on a planet that is perfectly suited for life as we know it is somehow perceived as a bigger challenge than making an inhabitable planet habitable.

Not the way you describe it but what you essentially think of is probably convergent evolution (http://en.wikipedia.org/wiki/Convergent_evolution)

It should be noted that gelatin is often used as a stabilizer for proteins, often used during freeze drying or other long-term storage procedures. As such they are probably a bit hard to get rid of, or would have to be replaced by something else that may be more hazardous. I would also like to emphasize again that severe reaction described in the Sakaguchi is very rare, (usually figures at around 2-4 per million patients) and, are more indicative of pre-existing allergies.

The largest amount protein in plasma (or blood in general) is albumin, which constitutes over half of the protein content (roughly 60%, though can be more depending on extraction method and measurement procedure) . Together with around 10-20 further blood proteins such as apolipoproteins, transferrin, fibrinogen, complement proteins, immunoglobulins they constitute about 95-97% of the total protein in blood. The salt composition is relatively simple in comparison and as John already mentioned, it would really depend on the use of the artificial blood. Whether it should functionally resemble plasma, or has retention qualities similar to it (e.g. for spike and extraction analyses). The latter would depend a lot on the type of compound under investigation, for example.

It is not really a mathematical issue but rather these equations describe chemical properties. The first is a model for enzymatic reaction, i.e. a simplification in order to estimate simple enzyme kinetics, whereas with the HH is for description of an equilibrium reaction useful for the estimation of pH based on known pka values. One does not really need to know mathematics (except very low level) in order to understand the equation and it is potentially distracting for some people to think of it that way. Rather just look at the involved the parameters. For instance, in HH you have the pka, as well the concentrations of the undissociated weak acid and the conjugate base. Looking at the equation it is clear that you have one constant for your system (pka) and then you just need to know the respective concentrations to calculate pH. Or if you know the pH you just need one concentration to solve for the other. It can also be used to experimentally determine pka, if unknown, of course. In a similar way, MM is a way to relate enzyme kinetics (reaction rates) to substrate levels. If things do not click it is advisable to figure out how far you understand those and start asking questions from there. E.g. is it how these equations were derived, or how these equations behave, how they are used, etc. As mathematically it does not go much about simple algebra.

Not the same way, though there may other complications, especially at high concentration. One thing is that it may be very rich in iodine, which could be a problem with sensitivity against it. There have been reports associating carrageenan with bowel and stomach issues but there is nothing definite, as far as I know. The problem with that is obviously that we have to rely on animal models, which may not represent humans conclusively. Moreover, for any problems that are not acute and have a rare occurrence within a population it is often hard or impossible to deconvolute all the factors that are involved (i.e. other components of the diet, existing allergies, genetic disposition, life style etc.). But going back to the question, it is not impossible, though it does not appear to happen frequently (at least with the dosages used as additives).

You are misinterpretating the conclusion. It does not mean that they had no allergies before (in fact the opposite is likely true) but that in five cases that had confirmation that they also had allergic reaction afterwards (they did not purposefully exposed them). The goal of this study is to link severe immediate allergic reaction to MMR, which is indicative of an existing allergy of the patient. There is no claim that I can see that any of it is causing food allergy. And again, the study design is aimed to look at pre-existing reactions. That is why they also surveyed whether there have been reported reactions to gelatine, to corroborate their findings on the IgE level. Be aware that the real issue is that many patients are allergic to gelatin, egg proteins and other components of vaccines and there are efforts to minimize them, One example are flu vaccines for popele with egg allergies. The link between the creation of allergies as an additional problem is not totally being ignored, however the links found so far are somewhat weak and would require more studies befire conclusions can be drawn (as being made in this thread). Note that the goalpost has been moved a few times within this thread, but the real intersting question are how likely are vaccines to cause (not trigger) allergies and how much their contribution to overall acquisition of allergies are. The truth is that right now epidemiological studies are being inconclusive, most likely because there is not a single most contributing factor that can be easily filtered out of epidemiological data. It is silly to purposefully claim that it is the case, however. That being said, the hygiene hypothesis is still a favored model by many. With respect to food allergies one theory is that delayed exposre may be a risk factor contributing to allergies and some ongoing studies (e.g. http://www.leapstudy.co.uk/LEAP.html) are looking into this.

Genes cannot be proven/disproven. Either a locus is getting transcribed, or it is not. If you want to find a linkage between, say, an allele and a phenotype (something further down the role), the experimental path would depend on the system/organism under investigation and the phenotype in question. E.g. phenotypes on the cellular level are more accessible to certain types of experiments as, say more complex and less well defined ones on the population level.

Coaches? Pffft they are just a distraction from the real issue. Rubber duckies!

The part that has is relevant is that that exposure to allergens (by whatever means) can cause allergies is some persons. Vaccines are obviously not exempt from it. However the vast majority does not appear to exhibit issues, indicating that there may be individual links that are worthwhile to explore. This is quite an endeavor and is likely going to take a long while until we elucidate the mechanisms and implement ways to diagnose it on an individual level (i.e. establish personalized medicine). However, to answer OP: It is because the benefits far outweigh any risk. The link to allergies are relatively weak (and as others pointed out there is not enough data to clearly link the rise of allergies with vaccinations on the population level), whereas the benefits are well known. On the same note you could ask why anyone would feed their kids peanuts, gluten, seafood etc. as they may at some point trigger allergies (or not). Or why do we dare to use cars as the toxins produced are well-known to have adverse effects on human health? Finally, it should be added that often it is not clear whether the kids may not only have a predisposition to food allergy, but may be already allergic for other reasons. In the cited study for example, they appear to have measured IgE only after having adverse effects. I.e. there may have been sensitized already.

Ouch. Well whatever the paper was about, it clearly demonstrates the dangers of self-medication with psychoactive drugs.

Generally the absence of oxygen would be beneficial (simple N2 would have the same effect) as anaerobic degradation is slower. Similarly drying at low temperature would be preferable. However, the key element is drying, as sufficient humidity would still allow for bacteria and other microorganisms to do their work.

Just to add, in the link above the autopsy of the keeper in South Australia was found to be inconclusive, whatever that means. With regards to the snake in Canada, the RCMP has described the (euthanized) snake as being 45 kg in weight (ca. 100 lbs) and about 4 m in length, so it is more likely to be a rock python, I would say. It would be odd if the kids were sleeping separately, but then the report mentioned that they were on a sleep-over, which makes it quite likely that they shared a bunk/bed/couch.

Agreed. The primary conversion is starch to sucrose btw (yeah sugar is often used to refer to non-polysaccharides, but somehow it I always feel that it is slightly sloppy when used in metabolic contexts... sorry for that) On a different note, it is slightly surprising how many papers exist that measure changes in bananas during induced ripening.

That book is quite good for a general overview, I used it quite a bit for undergrad level teaching. For some in-depth focus additional textbooks are usually necessary, however.

To add, as a rule of thumb, it is usually better to cast a wide web during graduate school, niche building usually starts during postdoc. Breaks in topics are not unusual and in some areas quite common. The main advantage of having a tighter focus is more that one has the opportunity to interact with a given community. But some are so small that it is tough to carve a niche within that community. For industrial work, some applied knowledge is usually desirable, but a lot also boils down to demonstrable people skills, rather than technical expertise. This is even true for positions that include tech support, product management and (especially) project management positions (I am talking mostly biotech and pharma here). It should also be noted that there disciplines that are much more theoretical than others. The key point is less the distinction between practical or theoretical (although of course wetlabs value the former more) but how skills can be applied to the question that a lab has. Also, problem solving skills are pretty much a prerequisite everywhere.

It would be a very atypical behavior. But the autopsy appears to be still out, so maybe some more info will be forthcoming. I guess one possible scenario is if the kids were sleeping in the same bed and the snake kind of strangled them together?

Disclaimer: this is not my field of expertise and only have tangential knowledge on this topic. From what I recall interaction betwen the hypothalamic-pituitary-thyroid axis and the GH=IFG-I system is rather complex and not fully understood on the mechanistic level. I.e. there is more evidence in terms of phenotypes rather than in the underlying regulatory circuits. As such there are conflicting models that try to consolidate these effects. That being said, I do not recall that TSH levels would lead to reduction of GHIH. The only model that I recall is that GH may promote T4 to T3 conversion and via that regulatory circuit (as T3 is more active). Also there has been indications that GH may influence TSH dynamics, but evidence is a bit shaky (often the data is based on GH replacement studies and additional factors may play in). For the opposite side (i.e. thyroid affecting GH-IGF-I axis) there is even less data (that I know of). One thing to note is that the stunted growth is not exclusively due to effects on GH but there is also direct effects of the thyroid horomones on bone growth, for example. One of the few studies that I recall (but I am not an expert in this field) have shown in mice that especially IGF-I is affected, and to some extent also GH. But again, I am unaware of studies showing in detail the molecular interactions.