Here is the news story with commentary here.
I followed the link to find that, as of 1999:
1) 70% of all US children were 11 years old or younger.
2) this group (<=11 yo) accounted for ~ 50 stereotypical kidnappings and ~ 10,000 "non-family abductions."
3) there were 2.5 times as many children older than 11 years old who were so abducted in 1999.
4) given the child population of ~70M in that year, and unrealistically assuming uniformly distributed risk (it's not), means that children under 11 would have a 1 in 10,000 chance of being abducted in the broadest sense of this study's definition and a 1 in 1 million chance in the stereotypical sense.
By comparison to the larger of these abduction numbers for <=11 year-olds, in 2010 roughly the same number of children died due to medical complications and about half this number died simply due to being in a car. These numbers include children up to 19 years old, so it's not a completely fair comparison. But I still think it makes the point: if you're against healthcare reform and are willing to put your child in a car, there's no rational basis for calling the cops on this woman.
In various online conversations I continue to post these and related mortality data because discussions about children rouse people's emotions, including my own, and data is helpful to ground/anchor one's sense of real risks.
Wednesday, July 16, 2014
Wednesday, June 25, 2014
What favors the evolution of drug-like molecules?
Placeholder - I've suggested to ASM that one session next year cover whether and how multicellular organisms exert selective pressure that favors the evolution of drug-like natural products. I plan to write more about this more, here, but for now this is what I submitted to ASM:
"Small molecules (natural products) transformed the practice of medicine, but we do not understand what evolutionary pressures yielded their important biological activities. In the case of commensals and primary pathogens, the host itself likely provides selection. How do natural products alter the host to favor colonizing microbes? Understanding this dynamic will crucially advance the prediction and measurement of novel activities."
I recommended these speakers:
Michael Fischbach
Nancy Keller
Gillian Turgeon
Christian Hertweck
Johnathan Walton
Any others you recommend for the session?
Monday, April 14, 2014
High-throughput scoring of yeast growth. Well - using 96-well plates, anyway
This is fantastic. Can't wait to get into the lab and try it out!
High-resolution Yeast Growth Curves in 96-well Plates
Abstract: To compare effects of screen compounds on various yeast strains, YPD yeast cultures were seeded from single colonies and grown overnight to saturation. The resulting cultures were diluted to approximately 1000 cells/µL and grown until log-phase was reached (absorbance of 0.6–0.9 at 600 nm). The log-phase culture cells were collected by centrifugation and washed twice with sterile water to remove the YPD media. The resulting pellet of cells was resuspended in the appropriate liquid media for the experiment. Cultures of 150 µL (1000 cells/µL) were deposited into wells of a 96-well round-bottom polystyrene plate. The plate was lidded and incubated at room temperature with continuous shaking and automated recording of the absorbance (600 nm) every six min.
We did a high-throughput screen last summer to evaluate activities of our pilot natural product library against millions of gene-gene interaction pairs in Saccharomyces. The idea was to map any activity of these compounds onto specific gene products (proteins). We have some intriguing leads that, if confirmed, could shed insight on the biology of the producer pathogen. The linked article article confirms my hopes that we can test whether hit activity reproduces in a high-resolution assay.
Thursday, April 03, 2014
Amgen scientists find 10% of preclinical reports reproducible
Still
a problem: in 2012, Amgen scientists reported that only ~10% of
"landmark" cancer precilinical pubs are reproducible. Predicating
careers on sexiness of results and novelty, instead of reproducibility,
is toxic to science and therefore to everyone who needs results that
work. See also.
"For example, showing data from tumour models in which a drug is inactive, and may not completely fit an original hypothesis, is just as important as showing models in which the hypothesis was confirmed."
That this needs to be broadcast to the field means that the incentive structure is broken. If all your data do not support the story you want to tell, and not for trivial reasons like "my puppy made those aliquots," then these are particularly critical inconsistencies to report. Whether you want to publish in Nature or Cell is and should be irrelevant - the data do not fully support the hypothesis.
In the end, it behooves no one to publish in Nature and temporarily boost your career while dooming months of subsequent postdoc work-hours to rediscovering the irreproducibility of your Nature-approved hypothesis.
"For example, showing data from tumour models in which a drug is inactive, and may not completely fit an original hypothesis, is just as important as showing models in which the hypothesis was confirmed."
That this needs to be broadcast to the field means that the incentive structure is broken. If all your data do not support the story you want to tell, and not for trivial reasons like "my puppy made those aliquots," then these are particularly critical inconsistencies to report. Whether you want to publish in Nature or Cell is and should be irrelevant - the data do not fully support the hypothesis.
In the end, it behooves no one to publish in Nature and temporarily boost your career while dooming months of subsequent postdoc work-hours to rediscovering the irreproducibility of your Nature-approved hypothesis.
Thursday, January 09, 2014
"Enterotypes" not so obvious after all?
An exciting possibility was that we could determine what "enterotype"
(collection of bacterial species in the gut) was associated with obesity
and, if causative, treat obesity by remodeling that enterotype to
resemble one that promoted lean individuals. This article suggests that
if enterotypes exist at all, we're going to have to look harder for
them.
"We find that inter-study variability in the taxonomic composition of stool microbiomes far exceeds differences between lean and obese individuals within studies. Our analyses further reveal a high degree of variability in stool microbiome composition and diversity across individuals."
Gotta love open access. Article via @iddux.
"We find that inter-study variability in the taxonomic composition of stool microbiomes far exceeds differences between lean and obese individuals within studies. Our analyses further reveal a high degree of variability in stool microbiome composition and diversity across individuals."
Gotta love open access. Article via @iddux.
Thursday, January 02, 2014
Arguing against vaccines can cause deaths
Vaccines
save lives. If you view yourself as a special case with unique
sensitivities to vaccines, and are inspired toward activism against
vaccines in general as a result, then you are morally obligated to ask
whether such arguments are worth humans.
Given data showing
that vaccines save lives, it follows that their negative effects are
smaller than the diseases they prevent.* Therefore advocating against
vaccination - rather than advocating for different formulations while
encouraging vaccination - is indistinguishable in effect from advocating
that people die from preventable disease. That's a direct
interpretation of what existing data mean.
* The conclusion is
that successful anti-vaccination arguments lead to more deaths. If
anyone has data showing that vaccine toxicity causes mortality at levels
approaching the diseases they prevent, please share. I don't care
about being wrong but really do care about accuracy. That said, note
that the above reasoning doesn't change with power of anecdote. Some
people have horrific reactions to vaccines. People also have horrific
reactions to whooping cough, hepatitis, influenza and smallpox.
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