Arete

Host specificity (the relative taxonomic range of a pathogen) is a result of co-evolution of pathogen virulence and host immunity. A pathogen affecting insects is less likely to affect humans than one evolved in rodents because of several factors. E.g. plant diseases and human diseases are almost entirely exclusive http://www.ourfood.c...pathology.html. as are the viruses affecting insects http://www.inhs.uiuc...ectviruses.html 1) A rodent body and a human body are considerably more similar than an insect body is to either - therefore a pathogen evolved to thrive in mammals is less likely to do so in an insect. 2) A pathogen is more likely to be able to evade a novel host's immune system if it is similar to the immune system of the host it naturally occurs in. 3) Adaptation to a novel host that is similar to the natural host requires fewer steps than a functionally distant host. E.g. I work on Trypanosoma brucei. T.b. brucei is only infectious in livestock. T.b. rhodesiense is infectious to humans. The inclusion/exclusion of a single gene is responsible for the ability of the parasite to evade the human immune system. http://journals.camb...line&aid=324617 4) Similar hosts are more likely to live in similar environments e.g. diseases affecting freshwater fish in aquaria are often distinct from those affecting marine fish.

Host specificity - E.g. a disease might be able to infect reptiles and birds, but not mammals. Another might be able to infect mammals and not reptiles and birds. Neither group has more diseases than the other, but they contract different diseases. Environmental specificity - E.g. A disease can live underwater but not above water, or vice versa. Many diseases of ornamental fish in aquaria affect only marine or only freshwater fish, due to environmental specificity of the pathogen. How long have scientists studied human disease compared to animal disease? How many scientists study human disease compared to animal disease? The answer is a lot longer and a lot more - which leads to ascertainment bias. For example - if I count hairs on the head of one person1 for a hour and get 3000 - then get ten people to help me count hairs on person 2 for a whole day and get 500 000 it doesn't mean person 2 is hairier than person 1 because I spent unequal amounts of time counting hairs - is that clearer? When fish and insects start investing in disease prevention, I'm sure there will be lots of money. While humans care more about humans not getting sick than fish/insects not getting sick, there will be a bias towards funding for human disease research. Most diseases are smaller than a cell. Once you become visible to the naked human eye, your actual size has little to no bearing on whether a disease will affect you or not.

In short - no. Genetically, anatomically and functionally speaking rodents and humans are similarly complex. We have anatomically largely have the same organs, mice actually have more functional genes than humans but they both share a goodly percentage of them (70~90%). It would be very hard to - in any rational, biologically founded way characterize rats and mice as less complex than humans. http://www.nature.co...-complexity-437 In a similar sense, characterizing insects as "very crude life forms" is hard to justify. Fruit flies have a smaller genome than most vertebrates and less genes, but this has little bearing on their relative complexity. Insect anatomy, behaviour and life history can and in a number of cases is more complex than most vertebrates. The anthropocentric view that humans are the most complex life forms on the planet doesn't ring true in a biological sense. Diseases which affect fish/insects in most cases do not affect humans and vice-versa due to environmental and host specificity of the pathogen, not differences in relative complexity. I'd think any evidence that humans suffer more disease than other organisms would suffer from rather severe ascertainment bias - we know a lot more about human diseases than animal diseases. Most of the famous rodent-human transmissions (bubonic plague, leptosporisis, hantavirus, etc) are a result of rodents and humans living in close contact, allowing pathogens which normally persist in rodents to transfer to human through insect vectors, contamination of human food and water with rat feces and urine, or direct contact - i.e. being bitten. This doesn't necessarily have anything to do with the same diseases you will get by coming into direct contact with waste - e.g. food poisoning via salmonella. However accumulated waste provides a resource for rodents, bringing them into contact with humans and thus causing transmission of diseases between the two species.

You let a stranger photocopy slides of unpublished ideas/data from your presentation?!?! If the English in the email is representative of the paper - this is a given. It will pay dividends to get an native English speaker to go over your work before submission to smooth out the grammar and spelling. I've had to review very poorly written manuscripts before and it's sometimes impossible to understand what was done and therefore critically evaluate the work, so it has to be rejected regardless of how good/bad the science actually is.

I did my MSc and PhD is Australia in evolutionary biology. I managed to publish 3 papers from my MSc (Two taxonomic revisions and a phylogenetic paper). The requirement for entry to a PhD program in Australia is (or at least was) a first class honors undergraduate degree or equivalent - publications can be used as an equivalent, so can a research MSc. Because I had a strong publication record, I had pretty good options when I went shopping for a PhD - I managed to find an adviser with a ready to go project and didn't have to find a stipend or research budget of my own. I finished my PhD and have managed to get ~ 8 additional publications from it (at least the ones in various submission stages). Again, my publication record came into play in negotiating both my wife (who is also in the same field of science) and me dual postdoctoral positions at a good R1 school in the US, which is where I am now. At least in my field and experience, your publication record is your benchmark as a scientist and the most important bit of your CV. Maximizing the impact and number of publications is something I have thought about a lot - I won't partake in a project that is unlikely to result in a publication and most of the projects are broken into blocks defined by the paper that will result from it. Advice on writing a paper: 1) Read, read and read some more. Get a good sense of how papers in your field are structured, what is topical, the methodological benchmarks and current knowledge. 2) Have an idea - look at your data and think about what it tells you and how to package that into a paper. I'd discuss your ideas with your adviser and get an idea of good/bad/feasible ideas for a paper. 3) Pick a journal - your adviser should definitely be helping you here. How high up the totem pole can you go? How good is the data, how topical is the idea? Do you want to aim high or be relatively sure of acceptance, etc. Once you've picked out a journal to aim for, print out the author guidelines and keep them next to you while you write the paper. 4) Write the paper. Easier said than done - make sure you do a bit every day, even if it's just a sentence to keep your head in the game. 5) Submit! Drink beer and wait... 6) More papers get rejected than accepted, so be prepared for a rejection. it doesn't mean your work is necessarily bad, it's a competitive world out there. You can always repackage your work and submit elsewhere. 7) Resubmit and wait. 8) Accepted! Drink Beer again! So in short, I think with decent guidance and motivation a MSc student should be more than capable of producing a publication and strongly agree that at least in the places I have worked, it would make a significant difference to how competitive you are for PhD programs and later positions.

What downstream analyses do you intend to implement? You can't really implement any rigorous phylogenetic or popgen methods without violating a whole suite of assumptions. Why have you dismissed using the data in its existing form with a suite of existing multivariate methods? It seems like you're re-inventing the wheel in the shape of a square here...

With Wikipedia? Really? "The models suggest that in impoverished families, 60% of the variance in IQ is accounted for by the shared environment, and the contribution of genes is close to zero" http://pss.sagepub.c.../14/6/623.short "IQ, is perhaps 48%; narrow-sense heritability, the relevant quantity for evolutionary arguments because it measures the additive effects of genes, is about 34%." http://www.nature.co...l/388468a0.html "large environmentally induced IQ gains between generations suggest an important role for environment in shaping IQ" http://psycnet.apa.o.../rev/108/2/346/ etc.

The posted figure was potentially to illustrate a point and not a literal depiction of a population bottleneck from 7 billion to 3.5 billion If you want to substantiate your claim with a simulation, download mesquite, model a panmictic population of 7 billion individuals. Bottleneck it to 3.5b and run the simulation until you get the same number of private alleles as before the bottleneck. http://mesquiteproje...e/mesquite.html This might take a while, but as a hint, a less extreme bottleneck in a population with Ne of 5, 000 results in a lower 95% confidence bound that suggests it would take longer than humans have existed for and an upper confidence interval suggesting it might take longer than placental mammals have been around for. Re: Asperger's. You still haven't explained why Hardy-Weinberg Doesn't apply to your proposal. Asperger's is recessive and seen in 0.003 (1 in 300) of the population http://www.specialed...er/asper11.html Using basic HWE, if p2 = 0.003, 2pq= 0.104 For every person suffering Asperger's, 35 people carry the genes causing the disease with no expression: by disallowing people with Asperger's from breeding with the general populous, you'll have a negligible effect on its expression. Repeating myself here - eugenics to eliminate genetic disorders violates basic genetic and evolutionary principles which I'm pretty sure are learned in high school and certainly are in the first week or two of Genetics 101. You can post repeatedly in this thread but you can't spend 15 minutes on Google Scholar to confirm or reject the fundamental assumption of your entire proposal? It's statements like the above that indicate eugenics is intelligent design for racists.

To the OP 1) the fundamental tenets are facts: a) There is standing phenotypic variation between individuals; b) Phenotypic traits are heritable; c) Differences in phenotype result in differential breeding success; d) Differential success of certain phenotype over generations leads to phenotypic changes in a population. e) When experimental allopatric populations undergo different modes of breeding success speciation is observed. 2) Evolutionary theory predicts genetic outcomes. E.g. the fields of phylogenetics, biogeography, molecular biology etc have put evolutionary theory to the test literally millions of times, and the prediction is accurate in a statistically overwhelming proportion of cases - thus it is the "least wrong" theory. 3) Application of evolutionary theory results in useful outcomes: e.g. vaccine development, selective crop breeding, biological control mechanisms, cancer treatments, etc. 4) Most of the arguments opposing are either logically fallacious, plain fallacious or based on a misunderstanding of the theory. 5) No alternative which explains observation based on naturalistic circumstances has been proffered.

Or not: http://biologicalsys...population.html You'll need to explain how basic population genetics does not apply to what you propose or it's nonsensical.

The premise is false. Selection pressure is not held temporally constant by evolutionary theory. Citation from literature needed. You've moved from logical fallacies to plain fallacy here. Fundamental evolutionary theory is not the subject of ongoing scientific debate. The observation that the sun rises in the morning is a lay fact, but a scientific theory explained by planetary orbits and rotation. In the same sense the observation of allopatric speciation is a lay fact and scientific theory explained by random mutation and selection. Please provide repeatable observation and significance values supporting your assertion. This statement is a "Russel's teapot" equivalent. The Genesis story is only supported by your own assertion it is true. The rest of your post is repetition of the same strawmen and false premises as the first. 1) The only temporal constant assumed by evolutionary theory is random mutation - selection is NOT a constant. Previously cited observation supports this assumption. Stochastic genetic drift is also an observationally supported phenomenon. 2) Evolution ONLY explains organismal diversification and change- it is not all encompassing like Creation. Evolutionary theory is unaffected by how the universe was created and how the first life forms on earth arose (your "seed" speculation). Disproving the big bang theory, or a novel bio-genesis theory has no bearing on evolution. Your insistence that it does is a misrepresentation. Being trite and rude doesn't help support your position. No one was demanding you "deal with it", calling your proposals "kid stuff conjurings" or questioing your reading and comprehension skills - you're doing yourself a disservice.

OP: 1) random mutation has been directly observed. 2) Selection based on phenotype has been directly observed 3) Differentiation of populations resulting in reproductive isolation has been directly observed. 4) An extremely large body of repeatable observation has been found to be consistent with the theory that random mutation and environmental selection dives organismal diversification. Ergo - held to the same standards as any other lay observation the theory of evolution is a fact. Joseph: a lot of your arguments are logically fallacious. 1) Speciation as defined by postmating isolation has been observed. http://www.jstor.org/pss/2410209 http://www.genetics....184/2/401.short http://www.annualrev...urnalCode=genet 2) The only "temporal constant" in evolutionary theory is mutation. Which empirical observation of data satisfies. http://mbe.oxfordjou...27/6/1289.short http://mbe.oxfordjou...4/12/2669.short http://sysbio.oxford.../59/2/119.short 3) The logic fails by false attribution - replace "evolution" with any other scientific theory describing a process longer than a human lifespan: e.g. Tectonics. If we can't measure plates constantly moving, by your premise, this theory (and numerous others) is false too. Strawman: Evolution =/= abiogenesis. Citing the need for bio-genesis does nothing to discredit evolutionary theory nor does it prove the Genesis story. Got a p value on the statistical significance of the Genesis story? If not, you're making an affirmative conclusion from a negative premise. Another false attribution - because an observation is not repeatable extra-terrestrially does not invalidate the observation. Replace "evolution" with the carbon cycle, or the ozone layer. By this logic, biology itself is not a science because it is not observed elsewhere in the known universe. Neither is tectonics, oceanography, etc and so on. Another strawman: Evolution =/= big bang theory. Questioning the validity of the big bang theory does not discredit evolutionary theory nor does it prove the Genesis story. Got a p value on the statistical significance of the Genesis story? If not, you're making an affirmative conclusion from a negative premise. Do you actually have any observational data to support this hypothesis? Argumentum ignoratum is not a valid logical premise. Strawman and argumentum ignoratum. Evolutionary theory does not state a "male" appeared and then found an exact female counterpart. There are many naturally occurring models of "genderproof" sexual reproduction. See bacterial sexual reproduction, situational parthenogenesis, temperature dependent sex and the biological definition of hermaphrodite.

This is nonsensical: Bottlenecks can and often occur in a single generation, which reduces both short and long term allelic diversity, and thus heterozygosity. Increased homozygosity is associated with increased incidences of genetic disease. http://www.public.ia...olEcolNotes.pdf http://www.jstor.org/stable/2387396 http://jhered.oxford...t/95/2/144.full http://www.mendeley....nary-potential/ http://onlinelibrary...050212/abstract http://www.springerl...r58412307k7517/ http://www.springerl...r58412307k7517/ http://www.nature.co...jhg201055a.html http://www.pnas.org/.../45/19096.short Rather than use IQ which is an environmentally correlated measurement of an arguable, multigenic trait (thus a rather idiotic measurement of intellect - as everyone's been telling you), lets show you how eugenics fails with genetic diseases. Let's say that the prevalence of an allele coding for a genetic disease is in 10% of the population. Now most genetic diseases are recessive and thus only expressed in homozygotes. So p=0.9 and q=0.1 p2=0.81 2pq=0.18 and q2=0.01 The ratio of undetected carriers to sufferers is 18 to 1. Eliminating people with detectable genetic disorders from the breeding population will be ineffective.

So to paraphrase - "Halving Ne (http://en.wikipedia.org/wiki/Effective_population_size)will have a negligible effect on allelic diversity." This is just not correct - it violates population genetic theory rather thoroughly.

An individual's genetic "fitness" in an evolutionary context is defined by the ability of that individual to maximize the quotient of their genetic information in the next generation. If she is able to maximise the amount of her genetic information in the next generation of humans more effectively than I she is genetically fitter. A species or population's genetic fitness is measured by its genetic diversity, as genetic diversity is indicative of phenotypic diversity, which is perceived to maximise the resilience of a population or species to environmental fluctuation. http://en.wikipedia.org/wiki/Conservation_genetics#The_importance_of_genetic_diversity Eugenic principles apply subjective values to arbitrary phenotypic traits and suggest artificially selecting for these traits. This, by definition reduces the genetic diversity of population and thus reduces evolutionary fitness. As an example, Pug dogs have experienced intensive selection for a desired phenotype. As a result they are extremely genetically depauperate - they have less allelic diversity than Pandas. The application of eugenic principles have led to an extremely evolutionarily unhealthy breed. http://www.nature.co...ature04338.html http://www.nature.co...epage&q&f=false

You just moved the goalposts: Individual fitness =/= differential population dynamics. Differential comparisons of "fitness" and "success" in allopatric, divergent populations is disingenuous to the topic of eugenics or individuals within a population. Look up population genetics: http://en.wikipedia.org/wiki/Population_genetics The argument is also entirely irrelevant with respect to eugenics.

Fitness is increased fecundity. Nothing more, nothing less, ascribing your personal subjective views of what a "fit" or "unfit" phenotype is to the theory of evolution is make believe nonsense which requires you to turf out all of the basic concepts of evolutionary theory. It's as illogical and stupid as Scientology. http://evolution.ber...eptions_faq.php http://www.talkorigi...hil/social.html http://autocww.color...lDarwinism.html http://www.pbs.org/w.../darwin/nameof/ Someone who has more offspring than you is evolutionary speaking - fitter than you regardless of them being dumber, uglier or less athletically capable than you. The environmental circumstances which led them to have more offspring than you is "selection". Your preconceptions of fitness have no basis in evolutionary theory and your subscription of them to is is make believe unless they have a demonstrable outcome on fecundity. Thusly, Social Darwinism is not "evolution put into a social context".

Again it's social Darwinism which is as much of misconception of evolution as Scientology is of science.

Natural selection doesn't simply stop because an artificial selective force is applied to a population....are you still arguing that natural selection doesn't apply to humans (which is demonstrably false - e.g. http://rheumatology..../6/485.full.pdf), or simply that your methods of selection a superior to nature? The impact of modern medicine on human suvivorship has no correlation to the supposed need for "intelligence" based selection - so it does little for your argument.

Given only 20.5% of people who complete a science PhD (i.e.. are trained as scientists) in the UK actually pursue a career in science, and a measly 0.45% end up as tenured academics, it seems like we actually have an oversupply of scientists as it is. http://tomhartley.po...m/r-e-s-p-e-c-t Do you actually have an evidence of this or is it pure speculation? More people are graduating university than ever before: http://www.lawsonry.com/698-the-devaluation-of-undergraduate-education/ http://www.educator.com/news/2009/why-your-college-degree-is-getting-devalued/ Natural selection cannot simply stop applying to a population of organisms; pick up a textbook and learn what the theory of evolution actually is. Fitness = fecundity, not your subjective interpretation of desirable/undesirable traits. Just because the traits you've subjectively decided should be advantageous do not necessarily result in increased breeding potential does not mean you get to bin natural selection. What you're proselytizing is Social Darwinism which is to Evolution what Scientology is to science.

Recombination happens within an individual: http://en.wikipedia....n_%28biology%29 (you'd move chuks of information around within a genome) Hybridization (Gene Flow) happens between individuals: http://en.wikipedia..../Introgression http://en.wikipedia.org/wiki/Gene_flow (you'd combine two genomes to produce an F1 hybrid) Both are routinely modeled when simulating genetic data for research (see above links) but again, it would depend on the level you're aiming at: trying to teach an elementary school class what recombination is probably won't go too well.

No they aren't. Scientific conclusions ARE theories which ARE supported by observation http://en.wikipedia....ientific_theory The Garden of Eden/ribwoman/talking snake gives away apples version of creation and Evolutionary theory cannot rationally be considered equally well supported and we shouldn't tolerate someone trying to teach children that they are. Respecting beliefs is one thing - pretending that they are all equally supported and viable is another. E.g. it's Johnny's right to believe the theory of gravitation is wrong and it's actually invisible shoe gnomes holding his feet to the earth, but should we allow him to teach it to kids as though it's as well supported as gravitation, or give him NSF funding to pursue the shoe gnome hypothesis?

This statement is incredibly useful in determining that the enunicator of it has no idea. Even if every single member of one generation contributed identical genetic information to the next (i.e. perfect neutral selection), which they don't - stochastic genetic drift would ensure that human populations will temporally diverge (i.e. evolve). Evolution does not "stop" and implying that it does conclusively suggests you have a very poor understanding of evolutionary theory. What you're actually saying is that you've: 1) subjectively determined the characters which you've decided should be desirable in humans; 2) assumed them to be heritable and not environmentally induced; 3) decided based on your anecdotal experience that these traits are not currently being selected for; 4) proposed draconian methods of ensuring their selection. Given your fundamental lack of understanding regarding the evolutionary process, the speculative nature of assumptions 1-3 and the ethical unacceptability of 4, the concept of eugenics you present and the subsequent actions you suggest are dismissible.

I'm not sure if this will help clarify but: Genome - the genetic material from an organism in its entirety. Gene - a sequence of genes which encode a protein. (analgous to a sentence in your simulation) Codon - a sequence of three nucleotides encoding an amino acid. (roughly analogous to a word in your simulation) whereas: Fragment - an arbitrary section of the genome, not specific to any functional purpose (e.g. for genomic sequencing we often shear a genome into small fragments using a mechanical method such as nebulisation to simply break the DNA up into manageable chunks.) To add to CharonY's suggestion, you could replicate recombination by moving sections of your alignment around, rather than simply modelling point mutations, but it would depend on how involved you want the simulation to be/it's intended educational audience and their level of background knowledge regarding evolution. It might also be possible to model hybridization between genomes... It might also be worth checking out how some of the actual nucleotide simulation software deal with such issues e.g. http://webs.uvigo.es/acraaj/GenomePop.htm http://mesquiteproject.org/mesquite/mesquite.html

I take the Eisensteinian viewpoint in that morality is a humanist concept independent of religion i.e. God doesn't tell us right from wrong, humans make that decision. There's interesting, well supported behavioral evolutionary theory which goes to explaining the rules of human societies and why humans sometimes choose to follow - and break those rules. A good book on at least the sexual aspects of such science is Sperm Wars by Robin Baker http://www.amazon.co...r/dp/0788160044 Because humans made up the concept, good is rather by definition relative. While on certain issues I'm sure the majority of us can agree on the "good" and "bad" perspectives to, there's always going to be grey on many others and thus, conflict between ideological standpoints. Whilst secular freedom of spirituality is in my humble opinion a very good thing, it allows a variety of dichotomous stances on virtually every issue. This isn't an inherently a bad thing in itself (and any scientist worth their salt should agree that viewing an issue from many perspectives and angles is often advantageous), until those differences of what is often fundamentally unsupported opinion are forced on others who choose to believe something else - which impinges on secular freedom and something I vehemently and passionately oppose (be it through legislation, sociopolitical pressure, billboards, TV ads or knocking on my door at 8am on Saturday morning - *insert bad words here*) and there is a "battle" we need to fight to preserve spiritual and intellectual freedom. Science and religion both try and explain how the world around us works - one is faith based and one is evidence based. Viewing it through the warped perspective of a scientist - it's not all that dissimilar than any other situation where there is two methods of investigating a problem. Sometimes the answer from both methods is the same, sometimes one method is more appropriate than the other, sometimes the answer from each is different and a judgement must be made as to which is more acceptable: and sometimes both methods return non-significant results... It reminds me a lot of the scuffle between nested clade analysis and statistical methods... http://scienceblogs....lysis_worth.php The problem is that science is by and large, is ideologically OK with the possibility of being wrong. This means that parts of scientific theory are allowed to be wrong and thus modified, and an entire theory can be dumped out in favor of a better one. In being faith based, most widely accepted religious doctrines are absolute - if part of the ideology is wrong, it's all wrong. This means that when scientific advancements contradict accepted religious doctrine inevitably lead to conflict. Whilst through apologetics, religion can be reinterpreted in light of scientific advancements and people (and religious organizations) can come to a point of reconciliation between the two methods, this is as a result of inherent and unavoidable conflict between methods of viewing the world around you.