*Emily Willingham at Forbes expressed some of these same ideas and then some over here. Please give that a read and let her know how great she is.
Anyone reading this blog knows that I am a scientist and that I am into politics. Currently, there is a debate happening in the scientific community about whether the March for Science that is planned for April 22 should be “political.” I think that the question is stupid. The March for Science is necessarily political. I think detractors question whether the march needs to be partisan, which is a separate question. Incidentally, I think the March for Science is necessarily partisan too. I want to point out why the march is necessarily political and partisan, and explain why I think the march–and what it represents–is important.
The March is being organized in response to a specific series of events. We did not call a march when Bush stopped stem cell research. This time it feels different though. We have a president who has openly doubted the value of vaccinations. He expressed skepticism toward the science of climate change. He showed disdain for the EPA and nominated a director who wants to dismantle the agency. The Trump administration’s habit of consistently disregarding the knowledge of experts seems to signal that he will try to govern without using empirical data to inform policy decision-making. Since this is a question of how our nation is governed, it is necessarily a political issue. The GOP has also made it clear that this widely-held belief among their adherents, making it partisan. As proponents of evidence-based policy, we are obliged to stand up to these decisions and the people making them.
None of this is entirely new or unexpected. We could have assumed that a Republican administration would lead to the same deregulation and climate science denial that was the hallmark of the Bush administration. The Republican Party has been denying the science behind climate change for years. But this is clearly a larger problem. Now we are litigating the value of vaccines, the EPA, and whether research will continue to be funded. Trump is the inevitable conclusion to years of conservative anti-science policy. Not content to just disagreeing on how to translate widely accepted scientific facts into policy, conservatives deny the validity of those facts and the experts who work to uncover those facts. The attitude of denying facts and questioning the motives of scientific experts reached its logical conclusion in the election of the authoritarian Trump, who eschews expert advice, norms of conduct, and the validity of facts. It is up to us–scientists and empirically-minded non-scientists, alike–to take our place in policy discussions. We should have been there all along, making sure that our worldviews were represented in the realm of public policy. After all, we are highly skilled professionals with a unique way of seeing the world. We have a lot of value to add to policy discussions. But many of us have neglected our roles as citizens. Now is the time for us to show that we have something to say about governing based on solid facts instead of a partisan agenda. Marching for science is a solid start.
It is probably easy to forget it with all of the baseball and politics flying around this page, but I am a biologist and that is what currently pays most of my bills. As a biologist, I do try to keep up on the interesting goings-on in my field, which happens to be somewhere between genetics and genomics. To that end, I printed out a research article about a week ago to read on the train, so naturally I just got around to reading it. The title, “A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns,” caught my eye because DNA rearrangement is something of an interest of mine. Little did I know I would nearly cry while reading this paper.
Pancreatic cancer is interesting among cancers because it tends to go undiagnosed until a relatively late stage. By that time, it is often hard to stop metastasis of the primary tumor to other organs, leading to a pretty short five year survival rate. Due to the loss of life that pancreatic cancer causes, it represents an active field of research. Specifically, a group in Toronto looked at the genetic changes that have to happen in a precancerous lump of cells in the pancreas in order to allow those cells to break from the main tumor and metastasize to other organs, which is how cancer causes the most damage. A popular model to explain the progression of pancreatic cancer dictates that a specific series of gene mutations has to occur in order to allow a precancerous cell to get to the point where metastasis can occur. Interestingly, this group showed that precancerous cells often did not exhibit the step-by-step accumulation of mutations that we thought would lead to metastasis. Instead, many tumors show signatures of simultaneous mutations that could only occur in the event of whole chromosome rearrangements. Which takes us right back to the DNA rearrangement that I am interested in.
Now let me address how I ended that first paragraph. I do not usually get emotional while I am reading papers, but I do not usually read papers that study case-by-case examples of patients who died of pancreatic cancer. It is incredible to think that there could be something growing inside you right now that will kill you in mere months or years. Tragedies like this are enough to make me not want to get out of bed in the morning, because what’s the point? Anything can happen tomorrow: “Pcsi_0410” was a real person with real friends and a family and ideas and a personality, but now they are just Figure 2 in a Nature paper. But I want to thank Pcsi_0410 for teaching us a little more about a terrifying disease that we all want to learn to treat more effectively. Maybe this is the only way we can make the best of pancreatic cancer. People are going to be unlucky and die from it, but we humans have been trying to make sense of shit like this for millennia. We will continue to try to solve the pancreatic cancer mystery, but we need people like Pcsi_0410, who were dealt a shit hand but use it to help others. But as scientists, let’s never forget the important sacrifice that some people have to make in order for us to get some cool sequencing data.
If you like to read the primary literature, check out the paper I talked about at Nature.
From time to time, I make a mistake by failing to keep up with the primary scientific literature as closely as I should. If I had been on my grind, I would have noticed that another Zika structure was published in Science at around the same time as the Nature structure that I blogged about earlier. The group that put together this structure also compared the Zika particle to related viruses, this time choosing to focus on a region of the viral protein coat that is especially dissimilar to related viruses. The authors go on to suggest that this region of the coat may be involved in attaching to host cells, which could explain how transmissible Zika is compared to its relatives.
(Image credit: Kostyuchenko et al. (2016) Nature.)
Update (4/27/2016): Science also published a Zika structure, drawing complementary conclusions from it. I thought it would be a good idea to post a small blurb about it here.
A group in Singapore published a structure of the Zika virus particle in Nature on Wednesday. Zika, which the Centers for Disease Control recently concluded is responsible for birth defects in children of infected mothers, has become a growing public health concern.
Victor A. Kostyuchenko and his colleagues at the Duke-National University of Singapore Medical School used cryo-electron microscopy to see the structure of Zika particles incubated at different temperatures. Importantly, the scientists found that the Zika particle is stable over a broader range of temperatures than other related viruses. On a practical level, this could mean that the virus is more transmissible than related viruses, and may be more challenging to control.
Virus particles are simply genetic material–either DNA or RNA–surrounded by a protein coat that protects and transports the genetic material. When the protein coat comes into contact with a susceptible cell, the virus can inject its genetic material into the host. The virus then uses its own genetic material to take over the cell’s own protein-producing machinery in order to produce more viruses. Eventually, those new viruses will be released and go on to infect other cells.
The authors note that their structural model can allow others to find drugs that may destabilize the virus. The hardiness of the Zika particle is almost certainly due to a tough protein coat, but certain drugs may make that protein coat more susceptible to degradation at higher temperatures or other harsh environments. All of this can be used to help stem the transmission of the virus.
For more information, check out the article at Nature: http://www.nature.com/nature/journal/vnfv/ncurrent/full/nature17994.html