Telling tales…

The following is an excerpt about the current interplay between science and the media, taken from an article in this week’s Nature by Colin Macilwain:

…thanks to the massive growth in public relations and to online media’s insatiable appetite for ‘content’, journalism in science, as in other spheres, has evolved into an ugly machine — called ‘churnalism’ by media-watcher Nick Davies and others. This machine delivers inexpensive and safe content, masquerading as news, to an increasingly underwhelmed public.

The machine prospers because it serves the short-term interests of its participants. Editors get coherent and up-to-date copy. Writers get bylines. Researchers, universities and funding agencies get clips that show that their work has had ‘impact’. And readers get snippets, such as how red or white wine makes you live longer or less long, to chat about at the water-cooler.

None of these groups is benefiting strategically from the arrangement. Science is being misrepresented as a cacophony of sometimes divergent but nonetheless definitive ‘findings’, each warmly accepted by colleagues, on the record, as deeply significant. The public learns nothing about the actual cut and thrust of the scientific process, and as a result is beginning to adopt a weary cynicism that can only rebound on science in the long run.

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A radical source of antibiotic resistance…

A FEW years ago, a Boston University team headed by Jim Collins published findings that suggested the means by which bactericidal antibiotics result in cell death. Rather than the cause being the cellular target of the drug, the team showed it was the secondary effects of stimulating the production of hydroxyl radicals, a reactive oxygen species 1. The hydroxyl radical is known to cause significant damage to cellular DNA, proteins and cell wall, leading to cell death.

Their 2007 study 1 was initially met with a few raised eyebrows in some quarters, coming in for some criticism for having a few gaps; namely whether the role of the hydroxyl radical was even pertinent in a real world infections settings, which are often in the low-oxygen environment of biofilms 2. There was also some question of whether it was adequately demonstrated that the oxidative stress was a source or the result of cell damage. However, subsequent studies reported by Kohanski, as well as other labs, have described a more defined link between a bactericidal drug and resulting hydroxyl radical formation 3.

In the latest edition of Molecular Cell, a new article from Mike Kohanski, Mark DePristo and Jim Collins reports that prolonged exposure to sub-lethal concentrations of antibiotics can induce multiple drug resistance in E. coli and Staphylococcus aureus strains that were initially drug sensitive 4. E. coli strains were tested with sub-lethal levels of  three major classes of bactericidal antibiotics (quinolone, B-lactam and aminoglycoside), which were found to significantly increase the mutation rate, confirming their expectations.

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Heat shocking adaptive evolution…

Research bloggingIN evolutionary theory there is a phenomenon known as canalisation, a process in which the phenotype (i.e. the outward physical appearance of an organism) remains unchanged, despite genetic or environmental influences.  This suggests that a mechanism exists to buffer the physical appearance from such changes, which may explain why some species can remain mostly unchanged for millions of years.

The buffering afforded by this mechanism permits the accumulation of genetic variation, in effect storing it up like an evolutionary capacitor. Also, presumably the accumulated genetic variation may be released by an event that overcomes the evolutionary capacitor, releasing fuel (in the form of variation) that provides a substrate for natural selection and potentially accelerating evolution. But how?

The idea of capacitance was first suggested by Rutherford and Lindquist 1 following experiments on a protein called heat shock protein 90 (Hsp90) in fruitflies. Generally speaking, heat shock proteins assist in the maintenance and correct folding of cellular proteins, especially when under temperature stress; Hsp90 plays a particular role in maintaining the unstable signalling proteins that act as key regulators of growth and development.

They suggested that in nature, a stressing event such as high or low temperatures may overcome the protective buffering effect that Hsp90 has on maintaining these key regulators. As Hsp90 becomes diverted from its usual role, due to an increase of stress-damaged proteins in the cell, those cell signalling proteins it normally maintains are free to adopt a range of altered behaviours, interfering with the development of the organism. The result is morphological variants upon which natural selection can act. Rutherford and Lindquist found as much, with chemically and environmentally compromised Hsp90 resulting in flies with abnormal wings, legs or eyes, they observed a broad variety of phenotypes.

Rutherford and Lindquist went on to demonstrate that the capacity for such remarkable variation was pre-existing, i.e. it was encoded genetically prior to the stressing event, but had been silenced. Evolutionary capacitance may therefore provide a mechanism of adaptive evolution in which a population under stress may release previously silent variation, resulting in the appearance of certain individuals with more desirable traits in that changed environment. When such revealed traits are selected for they can become fixed and independently of the buffering action of Hsp90.

This week, in a letter to Nature, Valeria Specchia et al.2 report some fascinating evidence that indicates that beyond merely acting as a gate-keeper to unleash variation, mutations of Hsp90 that compromise its functionality result in new, rather than pre-exisiting, variation. They observed that mutations in Hsp90 affect the production of piRNAs. These are small RNA molecules that are involved in the silencing of genes, particularly those involved in development, i.e. sex cells like eggs and sperm, and all the cell types that give rise to these cells. These piRNAs are also responsible for repressing genetic elements called transposons.

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Strategies for communication…

FURTHER to my recent post on why people don’t accept evidence, it turns out that an editorial 1 and an opinion 2 piece in this week’s Nature, the latter unfortunately behind a pay-wall, actually focus on just this issue. The editorial states:

“Empirical evidence shows that people tend to react to reports on issues such as climate change according to their personal values (see page 296). Those who favour individualism over egalitarianism are more likely to reject evidence of climate change and calls to restrict emissions. And the messenger matters perhaps just as much as the message. People have more trust in experts — and scientists — when they sense that the speaker shares their values.”

So people tend to accept the evidence that supports their personal proclivities, and in fact interpret evidence in a manner than does so, thus people tend to persist in cherished beliefs and views even when confronted with contradictory evidence. This of course is something probably appreciated by most of us. Dan Kahan, in his opinion piece, points out:

“People endorse whichever position reinforces their connection to others with whom they share important commitments. As a result, public debate about science is strikingly polarized. The same groups who disagree on ‘cultural issues’ — abortion, same-sex marriage and school prayer — also disagree on whether climate change is real and on whether underground disposal of nuclear waste is safe.”

Another factor that weighs heavily in the public perception, and acceptance, of facts is the messenger. Owing to the fact that most people are ill-equipped to evaluate the raw data from scientific studies, they rely on the position of credible experts; it seems that those experts laypersons see as credible are those perceived to share the same values.

Research into the mental processes involved in such public perception is, Dan tells us, being conducted by Donald Braman at George Washington University Law School in Washington DC, Geoffrey Cohen at Stanford University in Palo Alto, California, John Gastil at the University of Washington in Seattle, Paul Slovic at the University of Oregon in Eugene and Dan Kahan, the Elizabeth K. Dollard professor of law at Yale Law School. These processes are collectively referred to as ‘cultural cognition’.

So what is cultural cognition? Kahan describes it as, ‘the influence of group values (ones relating to equality and authority, individualism and community) on risk perceptions and related beliefs.’ I would imagine that peer-pressure represents one example within a spectrum of influences in cultural cognition.

Continue reading “Strategies for communication…”

Changing your beliefs…

FOLLOWING on from my post yesterday regarding people’s concept, or lack thereof, of evidence, it was suggested that it would be an interesting thought experiment for those of us who are willing to offer criticism on a subject to put ourselves on the receiving end. I think it’s a good idea to find something that each of us holds dear or true, and see if we can challenge ourselves to imagine how we’d feel if someone argued against that view. By understanding this, perhaps we can better approach our means of approaching such as subject with someone for whom such criticism would represent a paradigm shift.

As I managed to shake silly beliefs such as ghosts and ley-lines as a child, the only examples I have as a thinking adult are with particular scientific hypotheses that I’ve subscribed to, but subsequently had to ditch. This is the general method of science, and in my own research there have been any number of hypotheses I’ve formed and subsequently disproved on the basis of new evidence.

However, there have also been explanations for some natural phenomena that pre-date my research career, and to which I subscribed whole-heartedly. One example dates from my time as a first-year undergraduate studying marine biology. I had a particular interest in marine invertebrates and once attended a lecture by Donald Williamson, who was the major proponent of a larval evolution hypothesis, and recently came to light as being accused of ‘fringe science’ and getting a paper in the Proceedings of the National Academy of Sciences (PNAS) under the radar; thus also highlighting the pitfalls of the ‘I’ve got a mate in the club’ attitude to publishing.

Essentially Williamson felt that the immature forms (larvae) of many such invertebrates can be thought of as distinct organisms from the adult form, which are often comprehensively different both physically and physiologically; think caterpillar to butterfly, or blobby polyp jellyfish to its adult ‘medusa’ form.

Williamson felt that these different forms arose through hybridization — the fusing of two genomes (of two distinct organisms), one of which is now expressed early in an animal’s life, and the other late.

You can read an Sci. Am. article about it here.

I have to say, I absolutely LOVED this hypothesis, it was very exciting and I lapped it up with the typical fervour of an undergraduate.

Trouble is, since then it has been rebuked often and has not been substantiated by the experiments that were performed to test the hypothesis. I was quite recalcitrant about such rebukes up until the most recent PNAS rebuke that I’ve just linked to.

You can read rebukes to the Sci. Am. article here.

Changing my view about this hypothesis was hard, and a little embarrassing given I so animatedly communicated it to all my friends until I learnt it didn’t have strong grounding.

This is very true of many areas in which we are not experts, whether you are a scientist or not, and the fact is that we do tend to confer a great deal of trust in some individuals depending on their position. I would add that Donald Williamson was not ‘wrong’ to form this hypothesis at that time; scientific knowledge is by its very nature transitory, but once it has been tested, and alternatives developed, then we should seek to move on.

I could have easily ignored the evidence that Williamson’ hypothesis did not hold up to, and continued telling people an interesting and captivating story about why adult and juvenile forms of invertebrates are so different, but I didn’t. There’s still a part of me that thinks that there may still be something in it, which is why I can relate – to a point – with those people facing their first reality-check with regards some pseudoscience that they’ve hitherto believed in.

Donald Williamson is now retired and still stands by his hypothesis.

I don’t.

Your microbiome and you (part I): Gut

This post was chosen as an Editor's Selection for ResearchBlogging.orgYOU probably think that your body has things pretty much under control, being the finely evolved machine that it is, it knows where its at, and does a generally good job of looking after itself. You’d be right of course, but it doesn’t do this without a little help.

Some of this help comes in the form of your microbiome.

I have written previously about the exciting concept of the human microbiome in which I described how the number of bacterial cells on your body out number your own cells 10 to one, and asked to what degree you consider yourself to be human? The vast majority of these co-residents of you are organised into defined communities, the structure and diversity of which vary depending on where on the body they’re found: your mouth, your nose, various areas of your skin, your gut and urogenital tract. By understanding the interactions between each of these communities and our body, we can better understand their role in health and disease.*

In this the first of two posts on your microbiome, we’ll take a look at your gut.

The gut

probiotics-good-bacteriaMost people are undoubtedly familiar with the idea of ‘good bacteria’, in particular those of your gut, which we are encouraged to top-up on a daily basis with sickly sweet probiotic supplements containing various species of Lactococcus and/or Bifidobacterium. One can only imagine how on Earth we’ve coped throughout the course of evolutionary history without our daily supplement of Yakult.

The general scientific consensus on probiotics is that they don’t do any particular harm to most people, except perhaps your wallet, but occasionally the claims made by the manufacturers are often circumstantial, based on studies with poor methodologies, or are based solely upon observations from a petri dish or mouse model. Furthermore, when reliable evidence is documented, it is invariably for a very specific strain, thus there can be little confidence that is is a general property of the bacterial species as a whole.

Where the use of probiotics moves away from a general supplementation to being part of an active treatment for a condition, there is some evidence to suggest they may be of benefit, but on the whole, evidence is lacking and more research is certainly warranted. A Cochrane review (an international not-for-profit organization, providing up-to-date information about the effects of health care) in 2004, concluded:

“Probiotics appear to be a useful adjunct to rehydration therapy in treating acute, infectious diarrhoea in adults and children. More research is needed to inform the use of particular probiotic regimens in specific patient groups.”

However, in general there are insufficient data for the use of probiotics, over current standard therapies, in conditions such as eczema, Crohn’s disease, bacterial vaginosis and a slew of others. This is probably not helped by the fact that there is a good chance that the little pot of living bacterial joy you are consuming doesn’t actually contain any live bacteria of the type you think you’re getting.

A study published last month in the International Journal of Food Microbiology by an Italian team based the Istituto Superiore di Sanità in Rome, described a survey of such probiotics in Italy between 2005-6, seeking to identify and enumerate bacteria in commercially available supplements 1. A whopping 87% of samples showed evidence of not conforming to the Italian guidelines.

“Even though most labelled supplements (25 samples) indicated the presence of Bifidobacterium bifidum, this organism was only detected sporadically and always as dead cells.”

They also noted contaminants such as the food-poisoning pathogen Bacillus cereus, yikes.

Continue reading “Your microbiome and you (part I): Gut”