From Revere at Effect Measure on bacteria counts aboard commercial aircraft:
Shortly thereafter the news carried stories that the US EPA had determined that 15% of water on a sample of 327 aircraft flunked the total coliform standards and inspections showed that all aircraft were out of compliance with the national drinking water standards.
Too bad we can’t bring our own beverages any more.
Jim
I gave a talk for my friend and colleague Professor Margaret Polski at NDU today for her class on planning for what’s ahead in Afghanistan. Margaret is also an affiliate here at the Institute. I was delighted to find out that her mentor at Indiana was none other than newly minted Nobel Laureate Elinor Ostrom.
As a follow-up to the previous post, here’s an excellent essay on what’s gone awry for the field of nuclear physics over the last sixty years.
The story of nuclear physics is one of the most remarkable marketing disasters in intellectual history. In the space of a few decades, the public perception of the atom’s promise to serve humanity, and the international admiration that surrounded the many brilliant people who unraveled the mysteries of matter, had collapsed. So pronounced was the erosion of attitudes toward nuclear physics that, by the late 1990s, several European physicists felt it necessary to establish an organization called Public Awareness of Nuclear Science for the explicit purpose of improving the public image of their discipline.
I’ll have to put this one out to my theoretical physicist colleagues, but apparently there’s this wild idea that Nature is sabotaging the Large Hadron Collider to avoid creating a Higgs particle (which apparently gives things their property of mass). The notion is that creating a Higgs particle would be very bad.
I always enjoy Stanley Fish’s blog at the New York Times. Here he comments on a new trend for the courts to involvement themselves in the academy. It apparently used to be taboo.
They are according to NY Times columnist David Brooks. Read about it here.
This year’s co-winner of the Nobel Economics Prize, Elinor Ostrum works on a topic familiar to many Institute social complexity scientists: the tragedy of the commons. While this is a fascinating issue from the standpoint of human social behavior, I wonder to what extent our brain’s own cognitive resources (taken as a whole) are subject to something similar as we shift our attention from one thing to another. Isn’t cognitive overload essentially a tragedy of the neural commons? And is the entire cognitive attentional machinery a means of trying to avoid tragedy of the neural commons?
The Chronicle Review has an interesting article on Poker viewed through a kind of De Toqueville lens as integral the character of Americans. When I was in growing up in Pasadena as a Caltech faculty-brat Poker was a very important part of my socialization. My high school buddies and I played it with the intensity that I think some people ascribe more to chess–and we certainly weren’t playing for high stakes.
Background. Anxiety and mood disorders frequently occur following traumatic brain injury (TBI) and may influence cognitive and behavioral recovery. TBI involves both diffuse brain injury as well as frequent focal injuries to frontal and temporal structures, including the hippocampus and amygdala, areas that are associated with the neurobiology of anxiety. While there are anecdotal reports of response to selective serotonin reuptake inhibitors (SSRIs) in treating anxiety associated with TBI, no controlled trials have been conducted to establish SRSI efficacy in patients with anxiety following brain injury.
My major findings. I have been a co-principal investigator on two projects related to this proposed study: 1. An ancillary genetic study with a clinical effectiveness trial, Sequenced Treatment Alternatives to Relieve Depression (STAR*D), collected DNA from outpatients with non-psychotic major depressive disorder who received citalopram in the first treatment step in the trial. Participants were scored for treatment outcome and side effects. 2. An exploratory genetic study of individuals referred to the Walter Reed Army Medical Center and other collaborating military hospitals underwent a comprehensive TBI evaluation and were genotyped for polymorphisms in candidate genes involved in serotonin, dopamine, and glutamate neurotransmitter pathways. Comparison of mean differences among the genotype groups for several executive functioning measures was conducted. In the STAR*D study, a large population of patients with major depression (n = 4,000) treated with citalopram, we discovered and replicated an association of a reduction-of-function HTTLPR alleles to impaired SSRI treatment response. Furthermore, we found that side effects and treatment tolerability mediated this effect. We also identified a marker in the HTR2A serotonin receptor and a second marker in a glutamate receptor gene, GRIK4, that each predicted citalopram response in the same large patient cohort. In the TBI study, we determined that the e4 allele of the APOE gene (involved in neuronal plastic responses) predicted poorer memory performance while a variant of the naturally occurring Val158Met polymorphism of the catechol-O-methyltranseferase gene (COMT) gene, the Met 158 allele, which encodes an enzyme with reduced activity in metabolizing dopamine and norepinephrine, was associated with better performance on cognitive tests, supporting the idea that COMT Val158Met has a role in executive functioning, especially related to cognitive flexibility.
My aims and future plans. A goal of this study is to identify genetic components of behaviors following TBI. For example, decreased serotonin metabolism has been strongly implicated in controlling different behaviors in humans such as anxiety-related intolerance and impaired impulse control. In addition, because TBI results in the uncontrolled release of neurotransmitters, including glutamate and dopamine, both of these neurotransmitters are neurotoxic at high concentrations. Delineating the molecular mechanism of neurotoxicity acting through glutamate receptors (NMDA, NR1, NR2A-D; AMPA, GluR1-4) and dopamine receptors (D2) may provide sites of pharmacological intervention in protecting neurons from excitotoxic cell death. Envisioned is a randomized placebo controlled clinical trial of TBI patients treated with citalopram (estimated at 200 participants). Participants will be rated for improvement at weeks 3, 6, and 9 for possible dosage adjustment. Candidate genes and markers will be selected based on prior genetic linkage/association findings or neurobiological evidence from animal studies.
Relevance. The study is appropriate because a better understanding of the influence of genetic variation in response to treatment may aide in improving treatment regimens. It is likely that the future of patient care may rely on individualized therapies, where pre-treatment genotyping will be an essential part in the decision-making process to provide appropriate care and management of TBI patients.
Dr. Ruth Kirschstein passed away passed away on October 6. She was an icon at NIH serving 29 months as Acting Director in addition to serving as Harold Varmus’ deputy. All of us who are alumni of the National Institutes of Health will really miss her.
