Arete

Just like Ebola, Polio, HIV, Influenza, Rabies, Dengue virus, West Nile virus, Chikungunya virus, Zika virus, Marburg virus, Japanese Encephalitis, Congo hemorrhagic fever, Herpesvirus, Hepatitis, Rift Valley fever, Colorado tick fever, Ross river fever and of course SARS and MERS. All puny RNA viruses not worth worrying about.

I guess being trashy and tactless in reference to the death of a political rival is pretty on point for the republican base these days.

From a statistical perspective, your personal observations are anecdotes. That is not to say they are "wrong", but they are biased by your own personal predilections, where you personally travel, your habits, etc and so on. That is to say, that the observations of one individual, be it you or anyone else do not generate a representative sample. Non-representative sampling is statistically worthless. Further, purely correlative sampling is of limited worth - for a famous example, the increase in global temperature correlates with the decrease in the prevalence of pirates. I would say that using anecdotes about physical appearance to predict people's behavior would lead to a high degree of false positive and false negative results -and also a great way to amplify one's predilection for bigotry.

Speaking as a lab head, it doesn't matter what I think of your offense. For e.g. My lab has stocks of chemicals on the DEA restricted list. If someone has a felony drug conviction, I can't hire them. It wouldn't matter if they were the best molecular biologist in the country and their offense was smoking a joint at a Grateful Dead show in 1968, I legally can't hire them. If your conviction restricts you in a manner that prevents you doing the job (i.e. working with clinical patients) then no one can hire you to do it. Sex offenders are allowed to work on campus where I am, but have to register with campus police and face certain restrictions. My work personally doesn't face any of these restrictions and it would be illegal for me to not employ someone because of their conviction history.

I always thought it was a dimwitted plagiarism of Michelle Obama's "Be Better" slogan.

Only my armchair perspective, but the fact that a military-industrial complex with a $720 billion annual cost to the taxpayer, more than the next ten largest national military budgets combined, has bipartisan support requires the entire political system of the US to be skewed to the authoritarian right. If the US elected a genuinely left wing government, or genuinely fiscally conservative government, a level of demilitarization would inherently be a core policy, however the established political propaganda machine has made that position political suicide in the US. Most US Democrats would fall into the center right based on ideology and policy positions in most western democracies - I've lived in the US and it still boggles my mind that policies like nationalized health care are seen as a far left policy. Virtually every other western nation has support across the board for a universal healthcare system.

I hate the Nanodrop with a passion. So many failed library preps due to poor quantification - especially if you have any contaminants in your sample, which it sounds like you may. It's very simple and easy to use, but the data from a Qubit is superior - we just bought a Qubit flex, which takes 8 strip tubes instead of a single sample. Of course it depends on what you're doing downstream with your DNA - are you just doing PCR/Sanger, whole genome sequencing, cDNA, etc. If you're just doing standard PCR, Nanodrop data will be fine and save you a lot of time on gels, but if you're doing any sort of illumina/PacBio/Nanopore library prep, you'd want super clean extractions, like phenol chloroform extractions, and be prepared to have a high failure rate - which given the cost of library prep/sequencing kits, is going to make the $3K for a Qubit worth it pretty fast.

No one has ever turned into their cousin, or given birth to their nephew, so therefore no one is related to their cousins, nieces or nephews /s. If an organism spontaneously evolved into a distantly related species (fish into amphibians, flies into elephants, etc) our current understanding of evolution would be proven drastically wrong. The assumption of evolutionary theory is SHARED ANCESTRY. I.e. in the above example, that you and your cousin share the same grandparents, not that you can turn into each other or swap lineages. The evidence for shared ancestry is pretty darn strong - as an example, you share approximately 50% of your genes with a banana. That means you share metabolic pathways, cellular structures, developmental pathways, and many other life history traits that all strongly suggest that you share a distant ancestor.

Good luck fitting a toolbox in the tray though. I can see it as a mall crawler/toy hauler, but having just tied down an ls3 in the bed of my Frontier today and hauled straw on the weekend, I can see a lot of things that would have been troublesome with the design of this truck for actual truck use. I applaud them for the ingenuity, but I think it got int he way of practicality.

I'm not a US citizen but it seemed like the last election went a bit like this: "USA, this election you have to drink piss. We have this stale, slightly rancid cup of piss, very similar to the piss we've served for decades. It's not particularly palatable to many of you, but we know what we're getting and if you hold your nose as you sip, you'll be fine for the next four years. Or we have this big gulp of steaming walrus piss. It smells awful and it might give you syphilis, but honestly, we're really not sure what it's going to do." "Give us the Walrus big gulp. We're sick of being fed the same old piss. Drain the Walrus! Lock up the cup!" "OK..." Now we're three years into the Walrus piss big gulp. It's been a ride. Some of us are tripping balls and think the walrus piss is better than champagne, even though we might actually have mouth chlamydia and explosive diarrhea. Some of us hated it from day one. Many of us are not yet ready to go back to the same old, lobbyist corrupted, stale piss we had before, and want to swig more Walrus piss just to see where we end up. So now we're doing an MIC test on the Walrus piss to see if should even be an option.

I think it requires a rather profound misunderstanding of how science funding works to make that argument. To explain for those following - say I apply for a federal grant. The whole packet might be 50-100 pages of densely written technical documents. I will probably take me a month or more to put together. It has a 10-20% chance of being funded, and if it's a big one, might net $1 million dollars of funding. My institution immediately takes 55% as overhead. The vast majority of the rest will pay for the salaries of the people I employ. Some will go towards lab costs. If I'm lucky I might get to claim one month of summer salary (for the three months of the year the university doesn't pay me) for 3-5 years. Ergo, I might actually pocket a few thousand dollars at best. On the other side, Ian Plimer - a mining geologist who doesn't even work on climate science, pockets over $400,000 per year from the fossil fuel industry, and "coincidentally" is an ardent critic of climate change. If I'm going to make up data or espouse a false belief for profit, I'm sure as hell not going to be saying climate change is real.

One of the representations that has always bothered me, being a scientist, is that a "scientific consensus" is a bunch of us sitting around in tweed jackets, smoking pipes, sipping scotch and all nodding in agreement with one another. A scientific consensus occurs when a bunch of different data all converge on the same conclusion. Provided it's collected using best practices, data can't be political in of itself, it just, is

It's certainly not that clear cut. Conservation Science is a significant field of scientific study, with journals, societies, funding agencies. There are multiple scientific journals that publish studies specifically on the mitigation of climate change. There is an entire bureaucratic structure in most developed countries to provide scientific input to governmental policy decisions. Applied fields of science certainly do cross over with policy, and the line between science and policy/conservation/government is necessarily blurry.

Yes - you're right. In my lab we've been experimenting with disabling known resistance genes by inserting frameshift mutations to revert resistant strains back to susceptible phenotypes, but that is distinct from generating susceptible strains of inherently resistant wild type strains.

Artificial selection is not necessarily quicker than evolution, but using CRISPR Cas9 approaches, it is simple enough to produce antibiotic susceptible strains. Aseptic technique is still the most valuable tool in the prevention of nosocomical infection. Spreading pathogenic bacteria about an OR - drug susceptible or not, would have significant detrimental effects. So a few things 1) Often antibiotic resistance (AR) genes come with negligible costs to the bacteria, so do not suffer from negative selection. 2) They are often encoded on extrachromosomal transposable genetic elements (e.g. plasmids) or like the MecA gene in Staphylococcus aureus can be transferred by viruses - so you cannot prevent the spread of AR genes between your susceptible and resistant strains. 3) AR genes often, through selfish gene mechanisms, get crowded onto plasmids or prophage with other genes that confer a net benefit, such that they can piggyback on the positive selection of other genes to proliferate. 4) Resistance mechanisms like multi-drug efflux pumps, efflux many many other cytoplasmic contaminants, such they provided a benefit to bacteria in a wide array of environments. 5) Over 80% of antibiotics produced in the developed world are used as growth promoters in agriculture, rather than therapeutics. Therefore most of the interaction between bacteria and antibiotics is happening in the broader environment, not in the clinic. 6) Continuing from above, most of your patients present to the clinic having already acquired the resistant infection in the broader environment, so bacteria in the clinic are unlikely to have a positive impact. Dusting yourself with Staph/Klebsiella/Salmonella/Cholera etc, resistant or not is a terrible idea. You would wind up with far higher rates of infection and subsequent morbidity as a result, with a net negative public health outcome.

1. God is omnibenevolent 2. God collectively punishes humanity with genocide. Pick one.

If this is true, God let Nero, Genghis Khan, Ivan the Terrible, Stalin, Hitler, Pol Pot, Pinochet, Mao, Osama Bin Laden, Ferdinand Marcos, Idi Amin, Franco, Saddam Hussein, etc etc etc happen. Political leaders and regimes who literally murdered millions of people Why would the divine intervene in the 2016 election?

Significantly confounding problems with the simplistic approach you've taken include that mutation rates are not uniform between species and across genomes https://www.nature.com/articles/nrg3098 and that the number of observed mutations is proportional not just to mutation rate, but population size also https://www.ncbi.nlm.nih.gov/pubmed/17348929 Usually, to calculate time to most recent common ancestor (TMRCA), you'd use a molecular clock mutation model and a bayesian MCMC analysis to generate posterior probabilities. This article has a really good explanation of methods to calculate TMRCA https://www.genetics.org/content/158/2/897.

Strange already explained it, but the opening post sounds an awful lot like an irreducible complexity argument, and the factual errors, lack of citation and flawed analogies are archetypical of such arguments. To clarify, I'm not accusing you of religious motivation - but the opening post sure looks an awful lot like the standard lead up to a creationist pitch, which might explain some of the reaction you're getting.

You mean aside from the extensive discussion of regulatory function. Most of the eukaryotic genome does not encode amino acids. The original post failed spectacularly because it was riddled with factual errors and stank of religiously motivated creationist tropes.

Correct me if I'm wrong, but it seems like you're saying the "missing" information is that gene products conform to the scientific laws of nature in order to form biological structures... or are you implying that some unknown, supernatural other organizing force is necessary?

On its own - no. You brought up Hox genes in the context that the diversity of Hox genes did not account for the diversity of observed body plans. I simply presented the considerable body of empirical evidence which demonstrates that they do explain that variation. I hope this stems from a lack of understanding rather than disingenuity - but the proximity of a regulator to other coding genes dictates its effect in a regulatory cascade - no one should expect the Hox gene, or any other regulatory gene to self determine its regulatory function - genomic architecture dictates the genes downstream of a regulator. Hox genes are part of a regulatory cascade that does determine which proteins are expressed in cells, and how they differentiate spatio-temporally. They are part of the genetic system that governs "how millions of cells with different patterns of gene expression work together to create a morphological structure". I certainly did not state that Hox, or homeobox genes in general explain everything - that's a considerable strawman. "A diverse range of mechanisms, including nuclear dynamics, RNA processing, microRNA and translational regulation, all concur to control Hox gene outputs." https://dev.biologists.org/content/140/19/3951.abstract And here we go down the rabbit hole of shifting goalposts and argumentum ad ignorantiam. No one ever claimed that Hox genes in isolation explain the diversity of the tree of life, all of developmental genetics and the entirety of tissue differentiation. They are adequate to explain animal body plan variation, as shown by significant, already cited empirical evidence. The claim that they demonstrate a gap that genetics cannot explain was therefore false.

From your own citation: "Evidence in support of this last hypothesis has come from recent studies which document the overlapping function of different Hox genes [18], [19], and comparative studies of expression patterns in a number of crustaceans and insects [13], [14], [20] which support the idea that changes in Hox gene regulation may be responsible for the diversification of body plans and the generation of new segment types." Substantial research over the last 20 years has elucidated that spatio-temporal variation in Hox gene regulation and protein plasticity allows for an extraordinary array of body plans from the same ancestral set of homeobox genes. e.g. "A considerable body of evidence suggests that evolutionary changes in developmental gene regulation have shaped large-scale changes in animal body plans and body parts. In particular, many comparative analyses of Hox gene expression in arthropods, annelids, and vertebrates have revealed a consistent correlation between major differences in axial morphology and differences in the spatial regulation of Hox genes." https://www.cell.com/fulltext/S0092-8674(00)80868-5 https://onlinelibrary.wiley.com/doi/full/10.1002/bies.201600246 So, no, it supports the idea that developmental genetics underlies morphological diversity in the animal kingdom.

I appreciate you've though deeply about this issue - however this is incorrect. Regulatory genes can, for example, encode silencing mRNA which is used for post-transcriptional regulation of gene expression. RNA secondary structure can act to alter gene expression. Somatic V(D)J  recombination of existing genes is critical for adaptive immune function. There is an entire field of Developmental Genetics which deals with the mechanisms for differential expression during development - and the vast majority are genetically determined. Ultimately, the genome does a lot more than simply encode proteins, and much of its less obvious function is newly and incompletely understood - the term "junk DNA" was coined in 1972 to describe the 98% of the human genome that does not encode proteins. It wasn't until the 1990's that we started to unravel the function of non-coding DNA, but it does a lot more than we originally thought and were are still in the process of determining its function.