jp255

I agree with ringer here. Efficiency needs to be defined and should have been, but I will add some comments to the discussion. When I read the topic title I thought you were going to discuss whether or not the process of evolution in general is efficient. It seems to me the OP and his friend are not on the same page. The friend is arguing that evolution tends towards greater efficiency (for example, new allele compared to the previous allele of origin), so no arbitary level of efficiency is needed to call something efficient. An important point that has been raised already. Efficiency with regards to what? reproduction, survival, fitness, a combination of them? If anything efficiency should be an outcome of evolution, not a criterion of it. The efficiency your friend is arguing for is only possible because of the conditions required for evolution which is "individuals reproduce with variation which causes differential survival/reproduction" and "traits are heritable". So his argument should be "the outcome of evolution always leads to greater efficiency", or something similar to that. Although, it is possible for average fitness levels to fall over generations so I don't agree. Another way of looking at it is when you consider evolution as a heuristic search algorithm, which attempts to discover the highest fitness solution in the fitness landscape. Of course, this is purely theoretical and can't really be applied to nature as we do not know the shapes of the fitness landscapes. Consider it this way and efficiency could occur on two levels, the first is the speed at which it can find the optimum solution and the second is efficiency in terms of fitness gains. For the formor, the process of evolution is not constant and new evolutionary mechanisms have evolved over time so it is a possibility evolution has become more efficient in this aspect (hard to test). To the latter, it is possible that fitness levels can fall over generation (short term at least, and it is common for sexual selection to be involved).

http://www.ncbi.nlm.nih.gov/pubmed/16113465 http://ajrcmb.atsjournals.org/content/29/1/88.long The top one's ending remark is that inflammation isn't always necessary in the development of emphysema, though this doesn't really explain how emphysema is caused in the majority of cases. The second link offers evidence fthat demonstrates apoptosis and oxidative stress as contributors to the development of emphysema. Oxidative stress can lead to apoptosis itself, but I don't know if it acts predominantly by causing apoptosis in emphysema. They also mention in the beginning paragraph of the introduction that it was hypothesised that inflammation contributed to the development of emphysema from the observed association of smokers' lungs and patients on alpha-1 antitrypsin to emphysema. To answer your question, I do not know if inflammation has been demonstrated to be a contributing cause of emphysema. However, Oxidative stress and apoptosis look like good candidates, though I don't how much these mechanisms contribute to global/regional levels of emphysema.

Post in the homework section next time! I'd answer 2000 for the first one because 3 nucleotides = one amino acid. For the second one I'd answer 50% of the next generation would be hybrid. The previous generation were all hybrids that have one strand of 15N and one strand of 14N so the outcome after replication would be double stranded 14N/14N in one daughter and 15N/14N in the other daughter, meaning 50% offspring are hybrid.

Yes. I think the B cells will decline in number after the pathogen is killed off. A minority of those cells will become memory cells, which can respond quickly in the event of a future encounter with the same pathogen. This type of cell has a longer life span than a B cell, though I don't think they live forever otherwise there would be no need for booster jabs? I'm not totally sure on that but it would make sense. It would have to be the memory cells which would have to be passed on for long term immunity, and this doesn't occur as far as I am aware. However, the mother can pass on antibodies via the placenta and also via breast milk. The antibodies passed from mother to child are important, and help to protect against infection. http://www.ncbi.nlm.nih.gov/pubmed/12850343 http://www.ncbi.nlm.nih.gov/pubmed/22235228 Quoted from the first link: "Maternal milk antibodies coat infant mucosal surfaces and some have a clear protective role. This has been studied extensively in infectious disease models such as rotavirus, E. coli, poliovirus, and retroviruses. In the rotavirus model, antirotaviral IgA can be detected in stools of breast-fed but not bottle-fed neonates. In a large cohort of lactating women infected with HIV-1 in Rwanda, anti-HIV milk antibodies of the IgG isotype were more frequently detected followed by secretory IgM. Surprisingly, anti-HIV-1 SIgA were less frequently found. The presence of milk SIgA at 15 days as well as the persistence of a SIgM response during the whole lactation period was associated with lower risk of HIV transmission from the mother to the infant. Recently, HIV-1 antibodies from maternal milk have been shown to block transcytosis in vitro in a monolayer enterocyte model. Among these antibodies, those directed against the ELDKWA epitope had higher neutralising activity than serum antibodies. In humans, milk excreted antibodies play a major role in protecting infants from infection by pathogens having a mucosal portal of entry." I believe the protection received from the mother is temporary protection, most useful before the infant's immune system has developed properly.

Since the OP's question about specific usage of similar aas has been answered, I'll add some comments to the evolution of codons. The redundancy of the code is important and has some advantages. There are also some other advantages of the codon table that evolved which have been suggested from some evidence. http://genome.cshlp.org/content/17/4/401.long The above link is an interesting read about codon evolution. Some important points from the paper: 1) Codons can be reassigned (eg. a codon coding for glyceine is switched for another aa) and variant codes exist, suggesting the "frozen accident" theory (codons evolved to carry a specific aa, and from that point onward become fixed) is not possible. 2) similar codons are assigned to aas with similar properties, eg. polar aas. 3)codons do not always result in the specific aa it codes for (eg. glyceine codon can be mistranslated and lyseine inserted). This is called mistranslation 4) the genetic code is optimised with respect to minimising mistranslation (actual code has been compared to other possible codes) 5) there is evidence to suggest codon usage is biased to codons which can read as a stop codon if read off-frame (offers some protection against frameshift mutations by faster termination than other possible codes) 6) the codons carry more than just amino acid sequence information. Additional information can be carried alongside aa information such as splice site sequence, RNA secondary structure and nucleosome positioning. Seems to me the genetic code has been optimised by evolution somewhat.

Kind of. A wide array of antibodies will be produced in early B cell development, so we have a pool of cells capable of producing many many different antibodies with different epitopes (they will recognise different antigens). Production of more specific antibodies will occur during the adaptive immune system reponse to an invading pathogen. During this response a high affinity antibody (high affinity to the ivading pathogen's antigens) will be developed, and it is at this point when this specific antibody will become much more prelavent (temporarily). A bit like evolution on the micro level. The process is very much like evolution. Affinity maturation of antibodies by somatic hypermutation introduces variation. Then clonal selection of the highest affinity antibodies are selected, and then mass produced. http://en.wikipedia.org/wiki/Affinity_maturation http://en.wikipedia.org/wiki/Somatic_hypermutation Those pages are interesting reads. I find it interesting that this process, with it's striking similarities to the process of evolution, evolved. The evolved trait itself is like a genetic algorithm. Our immune system has evolved in a way that somewhat makes up for the vast differences in generation time between bacteria/virus and humans (minutes/hours vs years).

There are a number of factors which can contribute to the virulence of a particular virus. The type of cell which a virus can infect contributes to the symptoms an infected individual will develop. E.g HIV infects immune cells which has a CD4 receptor (a type of receptor the HIV virus uses to gain entry into a cell) so AIDs eventually develops, viruses which cause common cold symptoms infect cells in the nasal passage causing runny nose, fever etc. This is called cell tropism (the type of cell a virus has evolved to infect). The severity of the immune response that an individual's body launches against a virus can vary depending on the virus, and the location at which the immune response occurs can result in more severe symptoms. An example of severe immune response is the Spanish flu pandemic which is believed to have caused a cytokine storm (immune overreaction) in young people, which is thought to be the reason why it was most lethal to young people (unusual for a flu virus, usually kills infants or old people). The references for this can be found on wikipedia, just search and read about spanish flu. I don't know why certain viruses or strains can cause stronger immune responses. The location at which immune response occurs can affect the severity of the symptoms, eg rabies causing acute inflammation in the brain is very severe as opposed to common cold causing inflammation elsewhere. Lastly, some viruses have virulence factors. In viral genomes there is information coding for the required machinery to carry out the basic steps on the virus replication cycle. Some viruses also have additional genes which act as virulence factors. These genes can bolster the ability of the virus to infect and replicate. The mechanism by which these genes act is often by inhibiting the our defence systems. For example, We have APOBEC genes which have a function such that they can interfere in the virus replication process (e.g by introducing a lethal amount of mutations into virus genome). HIV-1 has a virulence factor which can disrupt this defence system (which is APOBEC3G, part of the gene family APOBEC) by degrading the gene's proteins. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1933301/ ,there are also other functions of APOBEC3G. Individuals infected with HIV usually die (eventually) primarily because the virus' mutation rate is at a level which allows it to evade the immune system, within one individual there are too many different mutants of HIV for the body to deal with. It is called a quasispecies. You can search many of the terms I used there to provide you with a lot of further reading if you wish to know more.

This does not follow from your original claim "13% of all men are gay". Why would you expect the bank scenario to be within the range 9-11% gay? You still havn't provided any support for your claims on what my opinions on the prevalence are. Putting words in my mouth. care to explain the relevance of this?

Care to provide some support for these claims? Do you think that by using those claims, my argument against your statement "13% of all men are gay" is invalidated? So 100,000 men were asked about their sexuality and the prevalence was 13% in this group. This 100,000 men represents a very small proportion of the total population, within which there are environmental, cultural and genetic differences. That is why I disagreed with your comment.

no it doesn't. It is limited to the particular population they studied. Why not just keep an open mind? there is a lot of research that still needs to be done. Polygenetic traits/diseases have been known about for a long time. Your possibility seems a little too specific to me, what makes you think incompatibility is the most likely cause of homosexuality if it is polygenic?

I'd consider this type of event to be a founder event rather than a bottleneck event. I think bottlenecks are when the population falls dramatically from deaths, and the Mars colonisation scenario is best described as emigration/reproductive isolation which is called a founder event. Doesn't change the outcome (Aliens from the film Mars Attacks!). The populations will go their separate ways.

That wasn't the progress I was hoping for. Why do you need any insight into your genetic code? you have already confirmed the causitive agent of your homosexuality. Or does this comment mean that you realise your assertions might be wrong? I would say you clearly have a naturally occuring trait. I think you're fit. I'm not keen on your attitude though.

Hmm? how do you come to that conclusion? Do I sense some progression? Only a few pages ago you were asserting your DNA had a mutation that made you gay, or does your case not fit into this group of "most cases"?

It is quite likely that there would be a loss of genetic variation. The likelihood increases the smaller the emigrating population becomes. The liklihood that some alleles will be lost and others become fixated also increases the smaller the emigrating population becomes. Since the population is small, it is likely there will be loss of variation. The rate of gene flow in this example (assuming the Mars inhabitants don't become prejudiced and decide to inbreed) is very small and will quickly become insignificant (occurs sometime after births exceed immigration). Assuming 20 years per human generation, only 40 people will come to Mars per generation. Depending on what assumptions are made, births exceeding immigration could occur over a small number of generations (the immigration would help to initially increase the population, but will gradually become less significant as the births will rise as a consequence). Since the gene flow is one direction only, the populations are destined to diverge over time (especially since the immigration rate will eventually be insignificant, once the population rises). Yes the founder effect question. It is a likely possibility. As for the other question, can gene flow offset the effects of genetic drift and the founder effect. I would say no when considering the scenario in the long term because the gene flow becomes insignificant. Gene flow essentially acts as a buffer between two populations, the more of it that occurs the more similar (in terms of genetic variation) the two populations will be. If anything, there could be partial compensation in the early generations (e.g an allele is lost by genetic drift in the next generation on Mars, but immigration re-introduces that allele), but the allele frequencies will not be restored to be the same as the original population on Earth (that will be down to genetic drift, more so as the gene flow effect weakens as immigration becomes insignificant). I have a feeling the term you used "Horizontal gene flow" will lead to confusion. "Horizontal gene transfer" refers to gene flow between individuals (e.g bacteria) from the same generation (i.e not offspring). So it's probably best to say veritcal gene flow, or just gene flow.

I understand your point, and agree. Couldn't you always just argue "their ability to critically examine their belief was not good enough" for any individual? and that no one is delusional when it comes to this type of belief? Is the scenario of an individual who is capable of critically examining their belief but doesn't possible? Is justification even required to form a belief? When iNow talked of stopping analysis of one's belief to maintain it, when someone becomes aware the foundations of their belief might not be true, is it right to still call it a belief? And what does delusional mean, and how does it relate to mental ability (doesn't delusional also imply that the individual is mentally impaired somehow, and so delusional is the same as inability in this discussion? are we arguing the for the same thing?)? I'm a bit confused now.

I'd imagine that the book would contain a definition of what the authors mean by genetic difference and what they include and don't include. By genetic difference, they could mean a number of things eg single nucleotide polymorphism, copy number variation etc. I am not sure which ones they are including or excluding in this extract. I think you are confused about sharing genes and genetic difference. They are not the same thing. We essentially share the same genes (most likely over 99.9%, not sure on the exact figure), but we will have differring alleles for some of those genes. For example, we both have the gene p53, but we might not have the same allele (version) of it. If we have different versions then that is a genetic difference. Genetic differences occur outside of genes also. Of those genes that we share, there are genetic differences of many kinds (SNPs, CNV, deletions, insertions etc.). The percentages in that extract refer to the percentage of all genetic differences (That the authors know of/are considering. The authors should have mentioned/defined this somewhere) across all of the shared genes. So, 85% of all genetic differences across all of the genes can be found in a population (don't know which they are referring to). 7% of all genetic differences across all of the genes can be used to differentiate between two populations within a "race". The remaining 8% can be used to differentiate between "races". I hope this makes the passage easier to understand. I really don't see how the authors came to that conclusion at all. Shame you stopped the quote there but I would not take those findings and conclude from them that the subspecies classification should be slain. The extract initally starts off with the term "race", which is fine as they did crudely define it. Making the jump from data concerning "race" to the conclusion of slaying the classification termed subspecies is not ok. It is also not justified.

I think opinions are quite important in a response, especially when it comes to interpretation of a paper. A stand alone summary of some research the expert finds isn't always the best answer. I'd always prefer a critical summary/appraisal with some input from the expert about the strength of the evidence/support (eg. limitations that are not mentioned, other opposing research), more so if I have little knowledge in the subject area. In such a subject area, I probably wouldn't be able to pick up on these additional inputs if I had read the original paper myself. Removing opinions from an answer would probably lead to more cases of misinterpretation, like misinterpreting suggestive evidence as proof. I don't know about you, but I'd rather input my opinion in an answer to minimise the chance of the question poster misinterpreting the research and I'd rather read an answer with opinions of this kind. I'd just like to add that conversing with people on these forums is an valuable way to improve your ability to critically examine evidence. Thinking about, and considering the expert's opinion and how they might have reached it, or discussing the evidence with them is worthwhile. That just gave me an idea, science courses at university should use forums like this for the purpose of improving critical appraisal skills, this is something I would have liked to have been incorporated into the course (in some respects I have learnt more in this forum than I did at university). Slight derail! but anyway, this wouldn't be possible without opinions.

Who is "we"? I don't share their view, whoever they are. What evidence? If you had used the definition which incorporates lack of evidence into it (as john responded), as opposed to evidence to the contrary, then those who don't bother to examine the foundation of their beliefs are included also. Not only is that definition better (evidence showing the non-existence of something is hard to come by), but also allows inclusion of those individuals. I do agree with that there is a generalisation. When you are scrutinising the belief of an individual, you just need to determine whether they have the ability to critically examine the foundations of their belief. After you have that information you can then proceed to describe them as delusional or not delusional. Agreed? They are very comparable in my opinion. Just pretend that someone is asserting the existence of the tooth fairy and compare it. There may be many pieces of evidence to support the existence of god, but they are all worthless in their ability to verify the existence of god. The amount of "evidence" there is to support the existence of something does not increase the individual value of each of the evidences. You can use this as a comparator: the claim from me that the tooth fairy is real. 1 piece of evidence vs 1,000,000's? they all have the same value. Which is ???????????.

I don't really get this part. How reliable would guided evolution mental faculties be? How could the existence of contradictory concepts even be explained in a world of people that have reliable mental faculties? It seems like the whole argument relies on the opinion at the end being true? That the probability below isn't necessarily true?

No, they don't always imply gain-of-function. They can result in haploinsufficiency. Also, mutations can be described using various terms, which appropriately describe their effect on function. http://en.wikipedia.org/wiki/Muller's_morphs For loss of function mutations, there are two terms. amorphic (complete loss of function) and hypomorphic(partial loss). For gain-of function mutations, there are three terms. hypermorph (increase in function), antimorph (acts antagonistically to the wild-type protein) and neomorph (novel function that is different to wild type function). dominant mutations can be amorphic or hypomorphic in nature. You missed out a number of modes of inheritance, mt, holandric, X-linked-dominant male lethal, co-dominance, etc.

In my opinion I consider the research to be preliminary, providing suggestive evidence. When I say, in post 50, that there is no evidence for it being a true cause, I mean that there are no identified causative epigenetic factors. The evidence currently only suggests that epigenetics could be a possible contributor to homosexual behavioural traits. It is for this reason, that the model is limited in it's ability to explain much at the moment. I disagree. That statement needs support by showing that the escape rate does not differ significantly across all human populations, or some other support. If there was variation in the escape rate, then it could in theory be subject to selection. If there was no variation then every individual would have an equal chance of having offspring with epigenetic escape, and so selection would not be able to act. The term "faulty" is inappropriate as previously commented.

With regards to the "counter intuitive" comment you made, I do agree that it is unjustified and unsupported. Also the article made the statement "From an evolutionary standpoint, homosexuality is a trait that would not be expected to develop and persist in the face of Darwinian natural selection", which is not only terribly vague but also unjustified or supported. The original paper cannot be used as evidence to support these assertions in any way, the model is barely in it's infancy and there is no evidential support for the underlying hypothesised causes of homosexuality. Homosexuality and it's contribution to fitness isn't totally clear to me, if you have evidence to support the assertion please provide it. you missed out an important word there "homosexuality might....", as I said the model is barely in it's infancy and there is no support for the model to be a true contributing cause. I think the issue with the usage of the word faulty is that suggests that the epigenetic transmission is by mistake. That would be unsupported. The author's of the paper leave it at "escape epigenetic erasure", not commenting on the nature of the erasure.

Thanks for that, definitely interesting. I wonder why you posted the article though. You should have just posted a link to the original paper, as that is always going to be more informative than a watered down summary (it is incorrect in places too, imo). The potential involvement of epigenetics seems to be a possibility. I would disagree with the statement that the study "solves the riddle of homosexuality". This study does no such thing (not even close), but rather it proposes a new model based on suggestive evidence of epigenetics and transgenerational epigenetic inheritance.

Thanks for that link. I wasn't aware of studies reporting evolutionary changes. It wasn't surprising that many of those traits had significant linear selection, since survival to reproductive age is likely. That individuals with lower total cholesterol, for example, had higher long term reproductive sucess, on average. So reproductive sucess is an extremely important factor when considering future human evolution.

In my point of view, nothing in the article supports the initial statement. The article is written in a way that (IMO) attempts to misguide people to the conclusion that ultrasound could seriously be harmful. No where in the article does she discuss the referenced experimental data and compare it to the way in which ultrasound is used to monitor pregnancies etc. For example, she mentions absolutely nothing about the intensities or frequencies. What if the settings were vastly different in the experiments? Also the paragraph where she mentions the VEGF stimulation and whatever else, the experiment itself was intending to investigate the cause of the therapeutic effects of ultrasound, yet she tries to portray these effects in a bad light and leaves the conclusion to "promotes growth" and then she states that "the effect is real". Yes, the therapeutic effect is real! The rest of the article is just as bad. She only supplies information which can contribute to the negative light she is trying to place on ultrasound and she makes no attempt to explain or discuss the "evidence". It is far from balanced, with the ending paragraph expressing a grave concern about ultrasound despite the lack of evidence. I'd be embarrassed to have my name on an article like that.