MicrobiologyBytes

There won’t be any formal clearing for Microbiology places at Leicester this year because basically, we’re full. (If you’re holding a place and haven’t responded yet, please contact us as quickly as possible.) The UK government caps the number of students we can take, although we do currently have room for a few more overseas (non-UK/E.U.) students, so if you’re interested in a place to study Microbiology or Medical Microbiology, please contact us soon.

Other than that, I hope you got the results you wanted, and we’ll soon be accepting applications for Microbiology places next year.

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Guardian University Guide 2011: Biosciences

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Over on our Facebook page, Heather Collins asked:

And another question – why do so few (UK) universities have microbiology departments these days? There’s been a trend towards bigger academic units, and disciplines who can’t recruit enough students tend to get merged with other departments into units usually called something like “The School of Life Sciences”. In addition, non-human microbiology is out of favour these days, with most of the money going to medical microbiology, and this killed off some microbiology departments who couldn’t or weren’t willing to adapt.

So why do UK universities find it hard to recruit microbiology students? When the A level syllabus changed a few years ago, microbiology all but disappeared. Actually, there is a little bit still there, but not until the A2 stage and it’s no longer offered by all schools. But A2 students have already filled out their UCAS forms. AS students don’t know what microbiology is, so why would they apply to do a degree in it? (They know what genetics is because there’s lots of that at AS level, so many apply to do that as a degree).

Fortunately, there is a solution! At the University of Leicester, we offer you not one but two chances to study microbiology. ”Microbiology” is a broadly based course including environmental microbiology, which “Medical Microbiology” is … well, see if you can figure it out ;-)

Of course, if it’s a bit late for you to be thinking about degree choices, we also offer lots of microbiology PhD and postdoctoral places, so check us out for all your microbiology career requirements :-)

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• MO Bio: 14 Reasons to Love Environmental Microbiology

Exactly 25 years ago today, Alec Jeffreys, Professor of Genetics at the University of Leicester discovered a technique that has subsequently had an incalculable effect on society, helping to solve criminal cases, resolve immigration arguments and clarify questions of paternity, not to mention creating one of the biggest civil liberties issues of our times. Working in the laboratory, Sir Alec recalls, he and his technician were simply following their noses. They had “absolutely no idea” of the applications that would result from the discovery they stumbled upon.

“I have never approached an experiment with a desire to solve a practical problem,” he observes, pinning down his moment of discovery to precisely 9.05am on Monday 10 September 1984. “My forensic thoughts at 8.55 on that morning were precisely zero; they simply were not there. The technology comes first and then suggests the applications, not the other way around, and you see this over and over again.”

But just as he has spoken out about the ethical and moral issues concerning the use of the technology he made possible, Sir Alec is a staunch defender of Britain’s curiosity-driven research. And the 25th anniversary of his discovery is, he believes, the right time to be discussing its future.

“As scientists, we have to be accountable to the public purse for the money we are spending, but if you take it too far – and in my view it has gone far too far now – it actually stifles the creativity of the very thing you are trying to promote.”

His warning is simple: applied science can be managed from the top down, but we apply the same approach to pure science “at our peril”. “It is blue-skies research that is the ultimate driver – delivering the new techniques, concepts and tools that we need to progress”.

Read more

Study at the University of Leicester

With the fall in H1N1 “swine flu” influenza cases recently, it has become fashionable for the media to run “What was all the fuss about” stories on the same page as “OMG, it’s going to be bad” stories. The problem with influenza is that it is one of the most unpredictable of all viruses, and while an upsurge in the number of cases can be expected as the winter flu season gets going in the northern hemisphere, the real concern is that this new pandemic virus might “turn nasty” in the second wave, just as in 1918 a much more pathogenic variant of that virus followed the relatively benign first wave of cases.

There are two ways in which this could happen. The first is that the present virus acquires spontaneous mutations which make it more pathogenic. The other possibility is that the virus recombines with a highly pathogenic influenza virus though the process known as reassortment – swapping of genes when two different strains infect the same cell. And there’s a good candidate for that out there – the highly pathogenic H5N1 avian influenza virus. Unlike H1N1, H5N1 has a hard time infecting humans, so it’s unlikely that these viruses would meet. But if they did…

The good news comes from Egypt, where H5N1 is relatively common, and a (worrying) case of H5N1/H1N1 co-infection was recently reported. The Ministry of Health has now discounted the rumour of a co-infection with the two viruses. In addition, a University of Maryland/NIH study suggests that co-infections of H1N1 with seasonal flu viruses do not produce chimeric or reassortant viruses. The H1N1 strain seems to outcompete seasonal viruses, possibly demonstrating this pandemic strain is not under biological pressure and is perhaps more efficiently communicable. Certainly, the past pattern seems to suggest that H1N1 pandemic seem to suppress outbreaks of other strains for some time.

A phase I clinical trial conducted by scientists from the University of Leicester tested 100 healthy volunteers with an H1N1 vaccine to see how their immune system responded. Trial leader Dr Iain Stephenson found 80 per cent of the volunteers showed a “strong, potentially protective” response after one dose, with more than 90 per cent showing the same response after two doses. The results suggest that one vaccine dose may be sufficient to protect against A(H1N1) swine flu, rather than two. Larger trials are now under way around the world involving up to more than 6,000 adults and children.

Reasons to be cheeful.

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“In my day” i.e. when I started my PhD back in 197<cough>, the first few weeks were spent joining the Enzyme Club. This encompassed all the biomedical researchers at the University of Leicester. Each new student would prepare a batch enzyme for recombinant DNA work. In my case, I made Hsu I (an isoschizomer of Hae III but allegedly easier to prepare). Since it was years ago, I can’t remember how many litres of the organism I grew up, but I remember very clearly doing the first assay on two litres of crude extract, and figuring out I was holding £40 million pounds worth of enzyme at the then current market prices. The first affinity column cut it down to £15 million, and a quick gel filtration to couple of millions pounds worth – still pretty good for two weeks work, especially when you remember that two million pounds was enough to buy you a house back in the 1970s!

Why did the Enzyme Club exist? Because these reagents were scarce in the 1970s, and rationed both by price and availability. Only a few years before, the only way to get hold of any of these enzymes was to make your own. This type of open science made sense. Why did the Enzyme Club cease to exist? Gradually, it became clear that the batch of enzyme I made wasn’t very good. It had a persistent exonuclease activity which meant it was fine for restriction analysis but rubbish for cloning, and it went off very quickly in storage, so that after three months there wasn’t much activity left. And although I’ve always been a rubbish protein chemist, that was a pretty common experience. Gradually, the companies dropped their prices and improved both the quality and availability of commercial enzymes. The day came when the Enzyme Club didn’t make sense any more, and it quietly died. It’s probably still moldering in the back of a coldroom over in the MSB.

So boys and girls, this is a story of the economics of open science, which made sense in response to scarce resources. When the availability of enzymes was limiting, this open approach made sense. When time became limiting, we all retreated back into our laboratories and got on with whatever we needed to do to get a PhD. The moral of this story is that open science pops up it’s head when times are hard and resources are scarce, but retreats quickly as the balance changes.

All scientific papers are important, but some are more important than others. Aside from its scientific importance, this paper is particularly important to me in purely personal terms. It comes from my own department. Ben Maddison was a PhD student in my laboratory many years ago and now heads up his own research group within the department. It’s also one of the final papers to come from Gary Whitelam, my former head of department, who died tragically last year. And as if all that wasn’t enough, as the UK starts to forget about how close we came to disaster with BSE, we’re still not completely sure that it’s all over.

Using the cutting-edge research technique of serial protein misfolding cyclic amplification (sPMCA), my colleagues show that prions are secreted in the milk from scrapie-exposed sheep. The sPMCA method involves incubating a small amount of abnormal prion with an excess of normal prion protein, so that some conversion takes place. The growing chain of misfolded protein is then blasted with ultrasound, breaking it down into smaller chains and so rapidly increasing the amount of abnormal protein available to cause conversions. By repeating the cycle, the mass of normal protein is rapidly changed into misfolded prion.

Since scrapie is not transmissible to humans, these findings do not indicate the likely introduction of zoonotic prions from sheep into the human food chain. Nevertheless, the data do indicate caution in the risk assessment associated with such foods. Although it is unknown if analogous shedding of prions into milk occurs with bovine BSE, evidence from previous epidemiological and bioassay studies suggests that such a scenario seems unlikely to cause clinical disease. However, the present report strongly suggests that given the importance of cow’s milk in the human diet the potential presence of low levels of prions within milk warrants further investigation. Analyzing milk samples by sPMCA offers a methodology with clear potential for the identification of clinically sick animals and those with preclinical/subclinical prion disease. Such a non-invasive, live animal assay has the potential to contribute to the epidemiological study, management and control of prion diseases within farmed animals.

Prions are secreted in milk from clinically normal scrapie-exposed sheep. J Virol. Jun 3 2009. doi:10.1128/JVI.00051-09
The potential spread of prion infectivity in secreta is a crucial concern for prion disease transmission. Here, serial protein misfolding cyclic amplification (sPMCA) allowed the detection of prions in milk from clinically-affected animals as well as scrapie-exposed sheep at least 20 months before clinical onset, irrespective of the immunohistochemical detection of protease-resistant PrP(Sc) within lymphoreticular and CNS tissues. These data indicate the secretion of prions within milk during the early stages of disease progression and a role for milk in prion transmission. Furthermore, the application of sPMCA to milk samples offers a non-invasive methodology to detect scrapie during preclinical/subclinical disease.

Related:

• Prions in Milk
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Applications are invited for a PhD Scholarship commencing in October 2009 to support research on the following project:

A new family of sigma-factor binding proteins; role and mechanism of transcriptional regulation.
Principal Supervisor: Dr Helen O’Hare, Department of Infection, Immunity & Inflammation.

The Scholarship will start on October 1st, 2009, run for three years and provide a waiver of University tuition fees and a student stipend equivalent to that of a UK Research Council award, £13,290 from October, plus an annual £1,000 research training support grant and £300 student conference/travel allowance. Candidates must hold a First or Upper Second Class honours degree (or equivalent) in a relevant discipline. This Scholarship is only available to candidates who are eligible to pay the Home/EU tuition fee, i.e. permanently resident in the UK or another EU country.

Further details about each project are available from the Principal Supervisor. Applications should be submitted as soon as possible by post or online.

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