CharonY

You overlook the second important function of red blood cells. What other gas plays a role?

If integrated into the hosts genome it is not longer directly infectious. Only the complete virus particle (RNA + Capsule) is. A chunk of genomic DNA even if containing viral sequences cannot infect you.

Well, check the properties of the respective amino acids (into what category do they fall, respectively) in each organism. This should give you the right idea.

The guys identifying the less specific restriction by EcoRI (the Boyer's lab, I think) termed the activity EcoRI* to distinguish it from normal enzyme activity. The asterisk was then later on translated to "star".

Annotation means assigning information to a stretch of DNA. Basically you only have the naked base pairs. Then you make ORF predictions (that is, identifying regions that might get transcribed), with further analyses you can then call it a gene and assign a function to it. The whole process, especially the latter part is called annotation.

Curation of gene sets of genomes loosely refers to overseeing, annotating or manipulating gene data (often manually). This may include: - fine annotation of genes - filtering of genes according to certain parameters - construction and manipulation of gene models and so on.

To be more precise LB is for the most part (10g) tryptone (tryptically digested casein) , half of it yeast extract (5g) and depending on formulation (Miller or Lennox) 5-10g NaCl. For agar slants you require to add 1.5 % agar into it. This is a so-called complex medium and not only E. coli, but also copious other bacteria and fungi will grow on it. Generally it is not a good idea to grow bacteria under these conditions, if you cannot work sterile, as you cannot exclude that you might grow pathogens. An alternative might be the use of minimal media (containing only the essential salts and vitamins) to limit unwanted growth, but this is far more laborious. In theory tupperware might work though. You have to thoroughly sterilize everything beforehand, and then use a large enough tupperware box. You only pour in a little bit if the medium into the dish so that you will enclose enough air if you seal it. If the box is large enough, there should be sufficent oxygen to grow some colonies. Still, I'd always advice to be careful working with bacteria.

DrDNA, if there were conductive and non-conductive nanotubes for reasonable prices (with a special focus on the price) I might actually be interested. Another problem with nanodots as labels, btw, is their ability to blink. Not few measurements screwed up due to this. In a way the phrase: "nanotechnology is the future" has a lot of truth to it. The majority is still is still in the area of basic research, meaning that only few of the current ideas will eventually hold water- in the future.

A problem with nanotechnology is that it has become a bit of a buzzword, similar to "systems biology". It lacks a coherent, stringent definition. In principle you can put so many things from different disciplines into that word so that it might essentially become (almost) meaningless (it just has to be small). In the few posts in this thread we have already seen examples of it. I could add plenty from the direction of biology and biochemistry. In scientific terms it is something under which you submit your grant application, if funds are available and you work with smallish things...

Let's put it like this, the species is the strongest possible taxonomic unit. However its universality is being questioned (especially in prokaryotes, though even in higher eukaryotes it is not that straight-forward anymore). As such it is unlikely that races are anything more than arbitrary distinctions with hardly any biological basis.

Actually the evolution of sex is far more complicated (mot to mention heavily discussed since the 80s). It has been stated that sexual reproduction would increase the fixation of beneficial mutations at different loci. On the other hand, there is little data that heritable variance of fitness is really increased by sex. In fact, recombination can lead to the breakup of favourable sets of genes and thus reduce fitness. Also, if all things being equal, an asexually reproducing female will have double the production rate than that of a sexual female. The latter is also the reason why tri-sexual mating is rather unlikely as it would increase the cost of sex even more. Overall to date there is no definite explanation why there is sex at all. More specifically it is unclear how sex initially evolved (as on its onset the additional costs should lead to its demise pretty fast) and how it is maintained. It is clear that it is a successful mode of reproduction, although quite a large number of animals and plants (not to mention prokaryotes) still reproduce asexually. A more molecular explanation stems from the similarity of the DNA repair and the recombination machinery. More recent evidence indicate that chromosomal recombination is in fact a by-product of DNA repair. As such ecological selection might play a smaller role than initially thought and chromosome maintenance selection might play an additional role. Spinning this further it has been proposed that sex originated from a form of genomic parasitism. Transposons, for instance rely on sexual recombination to spread and it has been hypothesized that sex is established to foster the spread of these mobile elements (selfish genes in action).

Actually I was quite dumbfolded when I first read that. Why should it be advantageous to die before getting cancer (dead is dead, you cannot reproduce either way). But after re-reading I am pretty sure that this statement is based on a simple misunderstanding (or maybe misformulating?). Essentially cell division (and cell aging) are strictly regulated (best known element is probably telomere shortening). In theory deregulated cells can divide longer and faster, though, which can reduce effects of aging. The downside is that this increases the risk of cancer. So essentially there is a trade-off between cell aging and cancer, with the mechanisms selected to maximize the overall reproduction efficiency of the organism. Death by aging occurs almost by definition later, when (as lucaspa pointed out) reproductive abilities were reduced (or absent), anyway. This is an example of the so-called antagonistic pleiotropy theory of aging, which states that pleiotropic alleles (in this case those controlling cell division) that increase survival/reproduction in early life but decrease the same at late life, can accumulate in a population because the selective advantages of the former outweigh the cost of the latter. Under the so-called mutation accumulation theory it is assumed that deleterious alleles can accumulate if their negative effects are confined to the old age when the selective forces are lower. If the first case was true that any change in genes involved in senescence will have an impact on early-life fitness (for example, increased cancer risk), whereas according to the second theory it would not be the case. As usual the in reality probably both effects play a role.

Essentially I agree with what the others said. Information gained by forced speed reading also tends not to stick into long-term memory. Reading regularly will increase your reading speed anyway. I heard that it might be worth to avoid regressions (involuntarily rescanning already read words), though. This on the other hand can also be achieved by regular reading.

Ouch. overlooked that part.

Hedges and Nowell, Science. 1995 Jul 7;269(5220):41-5 Further examples and elaborations were also given in these books: Biology at work – rethinking sexual equality by Kingsley R. Browne. Rutgers University press. New Brunswick ISBN 0813530539 Divided Labours – an evolutionary view of women at work by Kingsley R. Browne. Weidenfeld & Nicolson London ISBN 0297841408 Darwinism Today series. Series Editors Helena Cronin and Oliver Curry. A contrasting view was put forth in the commentary of the Nature magazine by Barres (Vol 442, 13, July 1996) Actually I read them mainly out of interest, but it is kinda helpful if you are a yourself in a position in which you at least have some influence about giving jobs to someone in science. As a male one can find oneself quite quickly in the sexist corner if one is not careful enough (hence I need good data, or at least literature).

Actually I would rephrase it to:"it could eventually lead to an adult human." While we would like to perceive biological processes in a fixed, mechanistic way, what is actually happening depends on a lot of things strangely not going wrong.

I stumbled over a rather old one: Wendy et al 1991

Nope, there is no evolution tree (using quotation marks doesn't make it better). At the very best one can envision an evolutionary bush with all extant species on the same level. Based on this the rest of the argument is pretty much moot. I am no expert in this field, but what I remember is an ongoing argument about the nature of consciousness (whether it exists, can be localized to brain areas, is an emergent property or not, the molecular basis and so on), and even more so on trackable markers for the same (e.g. language, tool usage and so forth). Based on this there cannot be any clear-cut, absolute separation of humans from other animals with at least a certain degree of brain complexity.Most argument discussing the "specialness" of human consciousness is based on similar arguments put forth by thedarshade: human cognitive abilities (and by extension, humans in general) are special, hence they are different. General consensus is that mammals apparently have the highest potential for higher levels of consciousness, although there are studies indicating that many birds also display behavior usually associated with cognitive behaviour (e.g. see Butler AB, Cotterill RM. 2006 Mammalian and avian neuroanatomy and the question of consciousness in birds. Biol.Bullet.). In the end however, there is not easy measurable marker (or even definition) that can be used to quantify consciousness.

The qiaex kit contains a protocol for the extraction of DNA from polyacrylamide gels, if I recall correctly. Essentially you need to let the DNA diffuse out of the gel matrix with a certain buffer, then you have separate the gel from the DNA solution (as it cannot be dissolved like agarose gels). The recovery rate was lower though. You can also do it without columns, but then you need to clean up e.g. by ethanol precipitation. Should work, but the recovery is likely to be even lower.

Technically you and your teacher are talking about similar things but on different levels. The process of DNA polymerization is dehydration synthesis, catalyzed by a DNA-dependent DNA polymerase. It is a part of DNA replication, but does not constitute all of the reactions that are required for in vivo DNA replication.

Indeed, especially in the light of modern genomic analyses. It is now (actually for a while) clear that for instance: - protein coding sequences are often phylogenetically older than the species bearing them (in other words, phylogeny of coding sequences does not necessarily correlate with that of the organism) - genomic DNA might arise from proliferation of DNA that have evolved to proliferate within genomes instead of benefiting the organism bearing them It is also clear that some of the implicit and explicit assumptions of the modern synthesis, including the assumption that the durable unit of evolution are in fact species, have been refuted.

I am not sure what you mean by that, to be honest. If one talks about immune response one usually refers to one of the many defense system an organism employs to combat other invading organisms. As such it cannot be viewed as symbiosis (which requires at least two different species). Regarding the transposon hypothesis: it refers to the adaptive immune response which specifically recognizes antigens and thus triggers specific immune reactions. The fascinating thing about it is that it can recognize an almost unlimited amount of antigens, despite the fact that there are only a limited number of genes, coding for antibodies. The trick is that the genes are shuffled to modify the antigen binding sites and thus generate the observable variance. The genes responsible for this shuffling are the so-called RAG (recombination activating genes) genes. The transposon hypothesis states that (based on sequence similarities) that the Rags were once transposase genes. A transposase is an enzyme, responsible for the transposition of certain mobile genetic elements, the transposases. So the theory states that initially early vertebrates possessed an innate immune system with non-recombining receptors for antigens. Then a transposon moved into the respective gene(s) and then was cut out again. However the second excision was imperfect (e.g. part of the receptor was also cut out), resulting in a modification of the receptor in question. This mutated receptor was then able to better recognize new or modified antigens and natural selection would favour the spread of this variant. Eventually this mechanism would evolve into the adaptive immune system known in jawed vertebrates. Other aspects of the immune response are far older, btw.

A very interesting if complex topic. One problem with a short answer is the overwhelming complexity of mammalian immune response, which is very multi-faceted. Regarding specifically the adaptive immune system, are you familiar with the transposon hypothesis?

It is a group of fungi generally found in guts of herbivorous animals and are members of the order of Neocallimastigales. There is also limited evidence that they are also found outside guts, though. Neocallimastix and Orpinomyces are some of the better known genera.

Your last question first: If you want to have tertiary structures, to date there are not many promising approaches. There are plenty algorithms for the prediction of secondary structures, though. For a collection of mostly older tools check expasy.ch Some use a combination of various algorithms like e.g.: Wallner et al. Nucleic Acids Res. 2007 Jul 1;35(Web Server issue):W369-74. Epub 2007 Jun 21. Ideally just search for papers in which prediction tools are presented and either they will describe the algorithm as well as the underlying prediction theory or you can check the references of said papers to get the information.