Latest Edition – Antimicrobials
This week has seen the SGM Spring 2012 meeting in Dublin. This was accompanied by an unprecendented (for SGM) level of activity on Twitter. (For those new to Twitter, I recommend the LSE Twitter guide for academics.) People who do not know each other can easily communicate on Twitter via a shared interest “hashtag”, in this case #sgmdub. So what can a closer look at the conference hashtag tell us about the meeting and the microbiology?
The Archivist provides some simple visualisations if the activity that went online paralleling the physical sessions:
The Archivist
Nice though the free Archivist service is, this is relatively crude approach to exploring and exploiting the data. To get a deeper understanding of the online interactions we need a three pronged approach:
1. Network
Via the generosity of Martin Hawksey I’ve had a look at some of the conversations which went on in order to make sense of them:
Visualizing the #sgmdub network
This provides the network view of online activity – the size of the names and the arrows indicate conversations. Click on the nodes (circles) in the live view for more information. This analysis also give a list of the Top Tweeters and Top Conversationalists using the hashtag. Finally, for the brave, here is a list everyone who used the hashtag (one spammer removed). What use is this? Use this information to find and follow microbiologists who use Twitter – the people you need in your Twitter network to provide and filter relevant information for your interests.
2. Content
For a summary of the online content the best overview tool is Wordle.net:
Visualizing the content of the #sgmdub hashtag
Of course delegates also talked about the weather, and I was pleased to get a personal mention. An edited view is provided by this Storify version by _zoonotica_. For the very brave, here’s the complete #SGMDub hashtag archive.
3. Context
Analyzing context is the hardest part. This cannot adequately be achieved from the network/content as it requires additional metadata, e.g. feedback forms – why did delegates say what they did?
Where do we go with this information? How do we continue the conversation now that the merrymaking in Dublin is over? I’ve already used this information to start talking to more UK microbiologists on Twitter than I was before, and I suggest you might like to do the same.
Please feel free to contact me if you want to discuss any aspect of this post further. And thanks for all those who contributed to a great conference :-)
On Monday I’m going to be at the SGM Spring 2012 Conference in Dublin (#SGMDub). I’m going to be talking about Social media for researchers – maximizing your personal impact:
Unfortunately this session clashes with the recording of This Week in Virology, so if you’re at the meeting, you’ll have to decide which session you want to go to. Hope to see you in Dublin :-)
Stanley Prusiner was awarded the first ever SGM Prize Medal (to a microbiologist of international standing whose work has had a far-reaching impact beyond microbiology) at the SGM Spring meeting at Harrogate on 1st April 2009. MicrobiologyBytes was there and this is a summary of his Prize lecture.
Prions are infectious proteins which multiply by binding to a host cell protein and converting it into insolubile fibrils (“amyloid“). Prions are associated with infectious, inherited and sporadic diseases – a feature unique to these entities. Tikvah Alper was the first person to identify prions in the 1960s, but when Prusiner started working on them in 1974, at first he didn’t believe the protein-only hypothesis. After eight years of failing to be able to identify any nucleic acid associated with them, in 1982 he changed his mind and invented the name prion (“pree-on”).
In prion diseases, the cellular form of the protein, PrPc, is converted into a disease-associated form, PrPSc. If prions really are infectious proteins, PrPSc produced in bacteria should be able to cause disease – and it does. It is also possible to produce synthetic amyloids with different biological properties – essentially strains of the protein.
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Quinacrine cures cultured cells of prions. In mice, the drug increases survival time of infected animals by up to 20%, but recently concluded clinical trials in humans have shown little effect. Prusiner’s group have found that quinacrine does work in stationary phase cells – such as those in the brain. Future trials of anti-prion (or amyloid) drugs need to be carried out in stationary cells. The latest assay uses genetically-modified mice which express luciferase when glial cells are disturbed. The resulting luminescence can be detected in the brains of live mice, and signs of disease can be recorded even before any neurological symptoms appear. This is up to eight times faster than waiting for the mice to die and examining their brains, and only requires one tenth of the animals. Prusiner hopes to use this approach to study Alzheimer’s and Parkinson’s disease, which also involve brain injury and amyloid deposits.
Stanley Prusiner’s take home message to all the students present was: it’s important to be lucky! But as Robin Weiss, SGM President, pointed out, Pasteur said: Fortune favours the prepared mind!
Related:
Links:
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ASM (Aus)
FEMS
SfAM
SGM
Internet for Microbiology
Small Things Considered
TWiV
Virology
