CRNA is Certified Registered Nurse Anaesthetist: they sometimes make as much or more than some primary care MDs.
CRNP is Certified Registered Nurse Practitioner.
Let me start by saying I love science. I love science so much I download podcasts like these and listen to them religiously. I also love science so much that I am 4 years into my PhD in molecular biology (hows that for vague? I guess you could call my specialty endothelial inflammation). I love my PhD program, I love my research, I love my lab, I love my boss (as grumpy as he is), I love my fellow grad students, I love scientists, I love it all! I even loved prelims. I hate failed experiments, but– the awesomeness that is science makes up for failure. However, the thing that the awesomeness of science does not make up for is being away from my wife and two kids. My 3-year-old son recently said, “Daddy’s home is his work.”
I, pardon my french, am working my ass off for my PhD. I don’t like to call it “work” because I love it, but I have yet to find a better term. Additionally, everyone around me is also working their ass off–no matter their career stage– and they’re better than me. So, in order to be at least as productive as them, I have to work even more. I have been doing science for quite a while now, and have yet to see “successful” scientists not put in 60+ hours a week. However, I have seen unsuccessful scientists put in 40. I chose science because I enjoy putting long hours into it, but after I got married and had kids I am now struggling with the balance of being a good graduate student and being a good husband and father. My Dad always said “these are the days you will work the hardest in your life,” but as I look at my boss, a successful scientist that puts in 12 hour days at least 6 days a week, I do not see the road getting any easier.
My question for the panel is this: Can you be a successful scientist and work a “reasonable” amount of time? I understand that some weeks may be harder than others– when grants are due and papers are in review and such. But I mean in general– can someone survive in science as a PI by only working 40-50 hours a week? If you do think it is possible, how? Do you have examples?
I have an idea, but I am curious if you think the people that review grants would fund a researcher this way. My strategy would boil down to two main points:
1. be the best at something
2. collaborate a lot
I figure if I am the best at something, then everyone would want to collaborate with me and we could trade experiments. Then we would be able to get more papers out with less failure that normally comes with troubleshooting an assay that is done infrequently. Is this a naive plan? Is it that currently funded RO1 investigators already do this? Are they already the best and they’re still working 60+ hours just to tread water? Would collaborations of the magnitude necessary for maintaining steady paper flow just be too daunting to accomplish?
Sometimes– to borrow a theme from Alice in wonderland– I feel like it takes all the running I can do just to maintain good status as a PhD student, and if I want to go on to a new role in science, I will have to run twice as much as that. I don’t have enough time to run twice as much. As much as I love the race, I am not willing to take more time from my family.
If you don’t think it is possible, do you have any other career options that may suit a PhD with as much fondness for science as me? If you do think it is possible– do you know of any good PI’s that may have room for a post doc in the next year or so that wants to study virus-endothelial interactions?
Thanks for your time,
FYI (In case you missed it).
Begin forwarded message:
From: ProMED-mail <firstname.lastname@example.org>
Date: December 12, 2012 8:06:11 PM EST
Subject: PRO/AH/EDR> Influenza (113): A(H3N2) receptor affinity change
INFLUENZA (113): A(H3N2) RECEPTOR AFFINITY CHANGE
A ProMED-mail post
ProMED-mail is a program of the
International Society for Infectious Diseases
Date: Tue 11 Dec 2012
Source: CIDRAP News [edited]
A study of the evolution of A(H3N2) influenza viruses since 1968 shows that the current virus has a low propensity to bind to human receptor analog sites, which correlates with the marked reduction in A(H3N2) disease impact in the last 10 years, UK researchers reported yesterday [10 Dec 2012] in the Proceedings of the National Academy of Sciences [abstract reproduced in part 2 below – Mod.CP]. The team used surface biolayer interferometry to measure virus binding to human and avian receptor analogs since the 1968 H3N2 pandemic. They noted that by 2001, the avidity of human H3 viruses for avian receptors had declined
4-fold, and since then, the affinity for human receptors also has decreased significantly. They conclude that this loss of affinity for human receptors “correlates with the marked reduction in A(H3N2) virus
disease impact” in the last decade.
Date: Mon 9 Dec 2012
Source: Proc Natl Acad Sci., early edition [edited]
Evolution of the receptor binding properties of the influenza A(H3N2) hemagglutinin. By Yi Pu Lina, and 13 others.
“The hemagglutinin (HA) of influenza A(H3N2) virus responsible for the 1968 influenza pandemic derived from an avian virus. On introduction
into humans, its receptor binding properties had changed from a preference for avian receptors (a2,3-linked sialic acid) to a preference for human receptors (a2,6-linked sialic acid). By 2001, the avidity of human H3 viruses for avian receptors had declined, and since then, the affinity for human receptors has also decreased
significantly. These changes in receptor binding, which correlate with increased difficulties in virus propagation in vitro and in antigenic analysis, have been assessed by virus hemagglutination of erythrocytes from different species and quantified by measuring virus binding to receptor analogs using surface biolayer interferometry. Crystal structures of HA-receptor analog complexes formed with HAs from viruses isolated in 2004 and 2005 reveal significant differences in
the conformation of the 220-loop of HA1 relative to the 1968 structure, resulting in altered interactions between the HA and the receptor analog that explain the changes in receptor affinity. Site-specific mutagenesis shows the HA1 Asp-225 –Asn substitution to be the key determinant of the decreased receptor binding in viruses circulating since 2005. Our results indicate that the evolution of human influenza A(H3N2) viruses since 1968 has produced a virus with a low propensity to bind human receptor analogs, and this loss of avidity correlates with the marked reduction in A(H3N2) virus disease impact in the last 10 years.”
In their discussion, the authors review the biological consequences of receptor binding variation as follows: “There are potentially important consequences of changes in receptor binding properties for virus isolation, for antigenic characterization, and for vaccine production. Viruses with decreased affinity for cellular receptors are under increased selection pressure when propagated in tissue culture cells and in hens’ eggs for vaccine production. Indeed, the reduced
avidity of the HA for the receptor is likely to be a key factor that promotes the observed ability of the virus neuraminidase to substitute for the HA in receptor binding by viruses propagated in certain cell lines. Difficulties with antigenic characterization derive largely from differences in the behavior of viruses in the hemagglutination assays that are central to antigenic analyses, leading to the need to use guinea pig erythrocytes in standard hemagglutination and hemagglutination inhibition assays for recent H3N2 viruses. Biologically, the most important consequence of amino acid substitutions that result in decreased affinity for receptors is their effect on the efficiency of infection and transmission. Despite the changes in receptor binding that have been observed, and the
widespread immunity to H3N2 viruses generally, these viruses continue to circulate and have predominated in North America in the 2010/2011 influenza season and in the 2011/2012 season in Europe. Nevertheless, it is striking that the severity of infections has declined since the major epidemics of 1968-1970, 1975-1976, 1989-1990, 1994-1995, and 1999-2000, and this may be linked to the marked reduction in receptor binding affinity in the recent years of this 44-year-long pandemic.
[These findings do not conflict with the generally held belief that human epidemic influenza viruses may arise by a change in their receptor binding properties such that the virus acquires a preference for human receptors (a2,6-linked sialic acid) in place of a preference for avian receptors (a2,3-linked sialic acid). In the case of the 1968 epidemic A(H3N2) influenza virus, however, this does not appear to have been a stable development, and, over subsequent seasons,
preference for human-type receptors has progressively declined. Definition of the evolutionary forces mediating these changes in receptor-binding properties of epidemic viruses will be an essential component in the analyses and prediction of influenza virus epidemics.
The practical consequences for vaccine production and antigen analyses associated with this decline in human (and avian) receptor affinities are considerable. – Mod.CP]
Hi Vincent and Crew,
I am a lay person with a keen interest in science, I have only recently discovered TWIP / TWIV and TWIM, and enjoy them all thoroughly, although TWIP is the easiest for me to follow. I really enjoy the back and forth banter between you and Dick.
I am a little confused about viruses and have a couple of hopefully not stupid questions:
1. If a virus infects cells in the body and integrates with the genome of the host, do they then become endogenous, or is it only if it infects the cells like sperm and egg cells
2. If a virus integrates its genome into a random location of the host’s genome, won’t it break the section of DNA that it gets inserted in the middle of .
I would love it if you could do an episode for new listeners with an introduction to virology, or even cell biology. If this has already been done, or you can recommend a suitable source for this information, it would be greatly appreciated.
I have started watching “Monsters Inside Me”, the TV Series that Dick mentioned in one of the TWIP episodes, with my 11 year old daughters, and due to my newfound knowledge on parasites and viruses I am sometimes able to name the parasite before they reveal what it is.
Keep up the great work, Cheers from Australia.
I don’t really have anything specific to say about this, just that I have a feel terrible heaviness in my heart.
Jason A. Roberts
Senior Medical Scientist
National Enterovirus Reference Laboratory
WHO Poliomyelitis Regional Reference Laboratory
North Melbourne, Australia
Dear Alan, Dickson, Vincent, Kathy, and Rich (in random order supplied by a random number generator*),
It is a drizzly 41˚F (5˚ Canadian) here today in Bar Harbor, Maine. I write you because I came across this article in Slate Magazine today that addresses flu vaccine skepticism:
Preliminary data suggests that this will definitely be of interest to your listeners (N=1).
I suspect that many of you are aware of the mainstreaming of flu vaccine skepticism. The author of the article is Dr. Darshak Sanghavi, a pediatrician and medical expositor. He starts the article by cataloguing several pieces in mainstream news and opinion sources promulgating skepticism of flu vaccine efficacy. He then attempts to dispel the skepticism by taking a historical perspective on infection control measures and shows how our current flu efforts rhyme with successful control efforts of the past. He goes on to discuss the idiosyncrasies of influenza and details how our current efforts to control it (vaccinations, Tamiflu, mandatory reporting of flu in children, etc.) are both a work in progress and also measurably better than the alternative.
Of particular interest to me is that he chose to cite primary literature to support his claims throughout the article, giving links for example to the British Medical Journal and the Morbidity and Mortality Weekly Report. This provides a good set of source material for framing the conversation about appropriate policy. But more broadly, this style of exposition shows tremendous respect for his readers intellect and, in my opinion, should be a model for science journalism, especially journalism surrounding public health matters. Diseases are scary and people, when confronted with them, will take the time and effort to get informed. Talking people through primary sources demystifies what scientists think and why they think it. That has real power to change minds.
So, at this point I will conclude by thanking you all for the TWIX series and your collective commitment to primary source news and opinions on pathogens of various types. I realize that you are not always discussing public health matters (nor do I think you should), but high-minded conversation about public health requires a sophisticated understanding of all of the issues. Influenza itself reminds us that controlling infections requires understanding multiple levels of organization from the molecules causing disease to the herds of humans swarming around the planet sneezing on each other (vaccines and Tamiflu in the small, herd immunity in the large). Each pathogen is different and complicated. Einstein apocryphally implores us to make things as simple as possible, but no simpler. An adequate public response to complex pathogens requires an adequate public understanding of their complexity. As such there is no substitute for adequate information and likewise no substitute for TWIV, TWIP, and TWIM.
My listener pick of the week is an article I found in Slate Magazine today… Oops! Recursive email!
I hope this letter finds you all well,
* MATLAB command ‘randperm’.