Arete

1) What is an "evolution tree"? Do they mean phylogeny? Given that they are generally constructed using nucleotide variations between species/individuals, it seems nonsensical to expect one for DNA. 2) There is no metric by which DNA is the most complex molecule in the universe. 3) DNA is reducible. It HAS to be reduced to RNA and individual nucleic acids to be translated. It wouldn't actually function if it couldn't be. The "meme" is therefore thoroughly incorrect and comprises a notably poor critique of evolution based on a complete lack of basic biological knowledge.

Even if the swab was contaminated with HIV, you would need a break in the skin of your mouth for any appreciable risk of transmission. Generally speaking it's SOP for a clinician to open any sterile swabs/needles/dressings in front of the patient, so you would have likely seen the swab come out of the sterile package it was in. As previously stated HIV has low viability outside of a host, so any contamination would have to occur immediately prior to you coming into contact with it. It's not like a malicious or negligent person could contaminate a swab, package it up at the factory and have it infect a patient days/weeks later. Any risk of HIV infection from a cheek swab is extremely negligible, even in a worst case scenario - even the risk of an infection following a needlestick with a needle known to be contaminated with HIV + blood is 0.32%

You cannot get HIV from a cheek swab

How do you explain the strong correlation between latitude and UV radiation levels? http://www.g3journal.org/content/early/2016/02/22/g3.115.026773.abstract How do you explain the fact that fair skinned individuals generate more vitamin D than dark skinned individuals following controlled exposure to UV light? http://www.karger.com/Article/FullText/354750 How do you explain the well researched trade off between protection from UV damage and vitamin D production? http://onlinelibrary.wiley.com/doi/10.1111/exd.12388/full

Personal incredulity is not an acceptable substitute for empirical evidence - again, could you please state the mutations in OCA2 you're referencing, so we can determine if they are fixed in the Caucasian population? This forms the very foundation of your claim, so it's important to establish for the credibility of your idea. I set out an empirically sound method to test your claim. Instead of making any attempt to follow that methodology, you've obfuscated and now stooped to ad hominem attacks. This tactic tends to indicate that you lack the ability to conduct such analyses, or grasp the critique of your proposal. A person of a scientific inclination would generally want to pony up the data to satisfy not just others, but themselves.

No, that's not what I said, at all. Please try not to shift the goalposts. Could you please tell us what mutations in the OCA2 gene you are proposing cause light skinned phenotypes?

It's not logical, its nonsensical. OCA2 is a) a gene present on chromosome 15 in the genome of all humans, and b) A disease caused by mutations in the OCA2 gene that results in symptoms characteristic of albinism. You statement, as quoted, doesn't make sense. Are you claiming that fixed mutations in OCA2 are responsible for the low relative melanin concentrations seen in light skinned human populations? If so, what mutation?

You just quoted two gwas studies that identified diagnostic SNP associations, That which is identified in Eiberg et al is in an intron upstream of OCA2 - so I'm not sure what you mean by "in vito and in vivo"... care to elaborate, given these are gwas rather than mechanistic studies? This is very different to identification of a causative polymorphism. Linkage disequilibrium and drift are plausible and possibly better explanations for fixed differences in non-coding gene regions. Are you discussing OCA2 the gene, or OCA2 the diagnosis? Everyone has the OCA2 gene, certain mutation thereof cause alibinism. Which mutation are you suggesting is fixed across the Caucasian/Hispanic/Turkish population, and causative of the phenotype? A SNP in an intron upstream of OCA2?

OCA1 is a disease associated with mutations in the GPR143 gene, OCA 2 is a distinct form of albinism associated with mutations in the OCA2 gene. There are no "stages" of Oculocutaneous albinism, there are multiple types with distinct, independent genetic causes.

So, you're asserting that mutation in OCA2 which confers a pale skinned phenotype, introgressed from India to Europe at some point, and subsequently became fixed? This explanation contains a series of testable predictions. 1) A diagnostic mutation/s in OCA2 is fixed in Caucasian populations. 2) This mutation/s confers the pale phenotype characteristic of Caucasian populations. 3) This mutation/s introgressed from Indian populations during (X) time. 4) The mutation/s swept to fixation since introgression. To test these, you would use the following methods: 1) Compare a sample of Caucasian OCA2 sequences to other human populations to determine the diagnostic polymorphisms. There's around ~50,000 OCA2 sequences on genbank, so this should be fairly straightforward. 2) This will be tricky without a model (e.g. a knockout line of mice) However, a first step would be to determine that the mutation/s detected in 1) are non-synonymous. 3) A coalescent model like IMa2 can be used to estimate migration rates and effective population sizes, allowing you to determine if introgression during the proposed time period is plausible. 4) A Dn/Ds calculation will allow you to determine the selection coefficient for any mutation/s you determine in 1), then a Brownian model like FPG can be used to determine the probability of fixation for the timing of introgression identified in 3), given the Ne estimate from 3) and the selection coefficient. Then you will have an empirical test of your hypothesis. Even better, all the software and data I've mentioned are open source, so there's nothing stopping you conducting the analyses. Some speculation, however: A) Given historical admixture between human populations, I would predict that the chances of finding a diagnostic mutation in OCA2 are pretty slim, doubly so now you've included Hispanic population in your hypothesis. B) Demonstrating functionality will be a problem - the evidence from the suggested analysis would be correlative and certainly not definitive. C) Based on other evidence I would predict widespread introgression between Europe and India, so I doubt this would prove troublesome to demonstrate. D) I believe that proving fixation is plausible in a reasonable time frame will be the death blow to your hypothesis. Human populations have very large Ne values (e.g 4% of the global population is almost 300 million individuals). Large Ne values, which necessitate very long fixation times even for genes with strongly positive selection coefficients. Good luck. Edit: Is there a reference you can provide for this? There a multiple diseases with convergent symptoms described under general term "albinism", however, I can't find any reference to any diagnostic "stages" of albinism.

So we just got a new sequencer in the lab I'm pretty excited to try out. It's a minION high throughput sequencer from Oxford Nanopore technologies and bless its heart it's cute! Supposedly capable of generating about 10 base pairs (bp)/sec for a total of about 110 million base pairs per run, it generates data in real time so you can stop sequencing when you have enough data for your experiment. It generates long (10-2kbp) reads, so we're hoping to pair it with our MiSeq to captialize on the strengths of both systems. It's dirt cheap for this technology at $1000 USD for the sequencer and set up kit, although consumables for it are pretty expensive. We're hoping to use it for investigating transposable elements in bacteria, and developing rapid diagnostic methods for clinical application. Let's see how it goes.

As a professor, I reluctantly agree.

1. Evolution, defined as changes in allele frequencies, through generations, over time, has been directly observed, many times. 2. Changes in allele frequency, leading to adaptation to environmental conditions has been observed, many times. 3. Changes in allele frequency leading to repoductive isolation between populations (i.e. the creation of new species) has been observed, several times. Ergo, it is a fact that evolution, as biologically defined, happens and drives the diversification of organisms. Furthermore, data is consistent with evolution being the only force involved int he diversification of organisms on Earth. A notable caveat is that this, of course does not exclude to possibility of other forces being involved in the diversification of organisms, however none (aside from the uncompelling, unquantifiable suggestions of supernatural guidance) have been put forward, and none are needed to explain our current observations. Your fish story, replete with inaccuracies as it is, amounts to a tale of personal incredulity - you don't understand how an aquatic ancestor evolved into a terrestrial organism does not mean it didn't happen or the explanation is inadequate. With all due respect and courtesy, it seems clear from your post that the shortcoming here is likely your understanding of evolution.

Keep the GPA up, engage in some activities outside of class (community service, sporting groups, clubs, etc)... potentially volunteer/intern in a research lab if possible/applicable and your goal is grad school - these are CV building activities. In order to write application materials, develop a plan for what you will do after college, in so much as you can. Grad school, then what? Start a company? Go into academia? A solid plan and demonstration that you're working towards it. Feel free to contact Vanderbilt admissions and professors to talk to them and ask for advice. Professors may be a bit hit or miss with responses, but you might get some solid, more specific advice. If I have time I often reply to those type of emails, but if I'm getting hammered that day they get left.

You sound like you're headed in the right direction, good luck!

Yeah, sure you failed out before. Is that going to have an affect on your chances - probably. However, far more importantly, what are you doing differently now? What's your GPA at community college? What positive things are you doing as well as school? Why do you want to go to Vanderbilt? What are you going to do after? What's plan B to get there is Vanderbilt doesn't work out? No one, especially not the selection committee at Vanderbilt wants to hear a "woe is me" story. As soon as you come across as a pity case, your application is going in the trash. Your posts are coming across as self piteous - if your future applications to competitive colleges have even a whiff of it, they're done. Making the selection committee feel sorry for you will not make them accept you. You need to get over the past and focus on how you're going to get to where you want to be. Selection committees are looking for students who can demonstrate a high likelihood of succeeding. Your need to demonstrate why that is you and focusing on past failures does the opposite of that. Demonstrating that you've faced adversity and overcome it may reflect positively.

I have some experience serving on a college admissions committee... Having failed out before is a red flag on your application - kind of like a past bankruptcy would be on a credit record. It makes you a higher risk applicant than someone without that on their record. With that said, if I was looking over your application, I'd be wanting to know you'd turned it around, had something to contribute to the college community and a clear idea of what you aspire to after college. Therefore, your chances will be reflected in: a) your current CC GPA (I'd guess that it would need to be over 3.5) b) your extracurriculars/life experience/community work/etc - what do you add to the Vanderbilt community? c) how concrete your post college plans are - you're coming in as a mature age student, so you should have done your soul searching and be on a path to something. How does a degree from Vanderbilt help, and how will you be an example of a successful alumnus? What will the press office be writing about you in the prospective student ads 5 years from now?

1) It's a common misconception that hominids evolved from other extant primates. We share a common ancestor - in a similar sense, you and you cousins share a common ancestor (i.e. your shared grandparents), but you didn't come from your cousins. 2) Even if humans did split from an extant primate population, there's no reason to expect that the ancestral population wouldn't continue to evolve along it's own independent trajectory.

Because freeze-thaw cycles can shear DNA, if you're using it a lot, keep it in the fridge. If it's medium term storage, -20, and I keep my long term stored samples in the -80.

No, I generally don't discuss the details of unpublished work on the forum. I sometimes post papers I have published in my blog, and generally do on my lab's website. My major point here is that things generally take several published studies to move from "speculation" to "experimentally supported speculation" and even more to move to "generally accepted hypothesis". It's typically not going to happen over the course of a thread on a forum, and is also beyond the capabilities of the average speculative forum poster to do it.

Just some perspective - I'm a collaborator on a project that involves some pretty novel treatments for multi drug resistant bacterial infections. We have multiple funding sources and are in stage 1 clinical trials, with some promising results. We've been somewhat hammered in the big 3 journals for our results being too speculative, and too preliminary. This after proof of concept in vitro, and proof of efficacy in actual patients in preliminary tests. In other words, multiple experiments and proof in the field is sometimes not enough for top accolades in science. Another example, the hygiene hypothesis is still regarded as a hypothesis despite over 25 years of investigation, is still regarded as a hypothesis and not a theory.

Another major issue is the inclusion of "0.03% chance of seizure (jerking or staring) caused by fever" for the MMR vaccine, but not for measles for two reasons: A) These are febrile seizures which, while frightening, do not generally cause any long term effects. They are therefore not generally considered severe side effects. B) They are caused by elevated body temperature. The fever caused by an attenuated vaccine is shorter in duration and less severe than that caused by the actual disease. Therefore an infant with the measles is at a higher risk of a febrile seizure than the vaccine, yet it is not listed in your comparison for both.

Quick buzz in the vortex, quick spin in the microfuge just to mix the reagents. Extensive spinning is not required.

I have both a Qubit fluorometer and a Nanodrop spectrophotometer in my lab for quantification. Which device do you have? The nanodrop takes a 1ul sample, so I generally just quantify a stock extraction. The Qubit seems a little more consistent, but is more involved to use.