Transferring Knowledge in the Horticulture Sector

1 05 2013

Horticultural Development CompanyI’m currently one month in to a three-month full time contract as a temporary Knowledge Transfer (KT) Manager at the Horticultural Development Company (HDC), while a colleague is on a secondment to DEfRA.

HDC is a division of the Agriculture and Horticulture Development Board (AHDB), a non-departmental governnment body that collects levies from farmers and growers in the UK in order to fund research into the industry. My role as KT Manager is to translate the research produced from the field veg projects that HDC funds into meaningful outputs that provide value for money for levy payers. In plain English, this means that I help turn science into practice – something that is of course right up my street!

Things I have been working on include:

  • Editing and proofreading field vegetables research projects
  • Producing posters (like these ones on post harvest disorders of peas and beans; see below)
  • Producing factsheets to help growers make positive changes in growing practices, based on HDC-funded research – currently working on a factsheet on carrot storage, and another on farmland birds
  • Writing press releases on newsworthy research and development
  • Writing articles for the next issue of Field Vegetables Review (to be published September 2013)
  • Publicising events and field veg news in the HDC Weekly Email and on the HDC website
  • Liaising with the University of Warwick and Syngenta to promote the HDC Pest Bulletin and Pest Blog
  • Publishing the monthly Brassica Research News newsletter
  • Writing HDC Research Update articles for the British Onions Producers Associations (see below), and the Brassica Growers Associations
  • Workig with Crop Protection experts to publicise the SCEPTRE project
  • [more to be added!]

When my contract at HDC is finished, I’m really looking forward to getting involved in more knowledge transfer projects, so please contact me for a discussion on how we can help each other.

Post harvest disorders of peas

Post harvest disorders of peas – (c) Horticultural Development Company/PGRO

Post harvest disorders of beans

Post harvest disorders of beans – (c) Horticultural Development Company/PGRO

British Onions newsletter April 2013

British Onions Newsletter – (c) British Onion Producers Association

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The Science Bit – Part 12: Breakthroughs in HIV research

25 05 2011

Research into finding the elusive cure for HIV, the virus that leads to AIDS, has been ongoing ever since the virus was first identified in humans in the early 1980s. Though treatment with highly active antiretroviral therapy (HAART) has dramatically improved such that the disease can be relatively effectively managed, HIV remains incurable and persistent.

Approximately 33 million people in the world are HIV positive, the majority of these in developing countries, particularly in sub-Saharan Africa. The virus, which is passed on through blood and semen, is able to cleverly evade the body’s immune system – hiding, in fact, within the white blood cells, the very cells that are supposed to seek and destroy viruses and other foreign bodies. Infection with the virus is practically symptomless, but left untreated, as the virus gradually proliferates inside the body, it overpowers the immune system and leaves the body susceptible to opportunistic infections that the patient is unable to shake off. It is this Acquired Immune Deficiency Syndrome (AIDS) that leads to death, via secondary infectious diseases such as TB, pneumonia or viral cancers.

Antiretrovirals – drugs which attempt to slow the replication of virus particles inside the body – have improved the quality of life and life expectancy for HIV positive people (who have access to these drugs) no end. Though someone with HIV will, likely, ultimately die of an AIDS-related disease, they can be expected to live a long and relatively healthy life, as opposed to a death sentence within a few short years as was previously the case. Recently, a research team from the National Institute of Allergy and Infectious Diseases (NIAID) in the US has demonstrated another important benefit of antiretroviral therapy – that starting HAART as soon as HIV infection is diagnosed, rather than when AIDS begins to become apparent, can actually reduce the ability of HIV to spread from person to person.

From a huge randomised clinical trial that began in 2005 and spanned 13 countries around the world, it was found that cross infection with HIV to a non-HIV positive partner was 96% less likely if the HIV positive partner began taking HAART while their immune system was still healthy, compared to patients who began HAART only when their CD4 T-cell count fell to below 250 cells/mm3. In fact, in the first study group, only 1 new HIV infection occurred, compared to 27 in the latter group.

And NIAID are on a roll, it seems. Another research group investigating the possibility of a vaccine for HIV infection have made a very significant breakthrough using a monkey model of infection. A potential vaccine for SIV – the simian equivalent of HIV – was trialled by giving half of a healthy study population of monkeys an injection containing the vaccine, and half a placebo. The monkeys were then injected with one of two strains of SIV. Unfortunately, the vaccine failed to protect against those given the SIVmac251 strain, but of those given the SIVsmE660 strain, 50% did not develop SIV infection.

Though of course, it is too soon to tell whether this vaccine will work equally well in humans with HIV, the results are very promising. By studying the blood cells of monkeys used in the study, the researchers were able to identify the effect of ”neutralising” antibodies that helped to prevent the SIV virus from replicating, and so affirm that this line of enquiry into an HIV vaccine is valuable. The best previous vaccination results were from a study carried out in Thailand, and that particular vaccine conferred only 31% protection against the virus, so it is clear that while a cure or a fully protective vaccination for HIV is still far away, we are certainly moving in the right direction.





The Science Bit – Part 11: Resisting Antibiotic Resistance

30 04 2011

There’s been a recurrent trending topic in the scientific community’s Twitter feed in the last week or so – the increasing problem of antibiotic resistance and in particular, the isolation of a new superbug gene that could be coming to a hospital near you very soon. But what are these so-called superbugs, how did they get here, and how are we going to stop them?

Superbugs are, in short, strains of bacteria that have evolved the ability to be unaffected by antibiotics – the drugs that we use to kill them and prevent the spread of infection. The superbug that most people are most familiar with is MRSA. This stands for “methicillin-resistant Staphylococcus aureus”. Staphylococcus aureus is a very common bacterium that is often found living happily on our skin and up our noses without giving us any grief. It usually only causes problems if it gets somewhere that it shouldn’t be, like into a wound, and if that happens, a trip to the GP and a course of penicillin will usually see you right. MRSA however is a strain of this normally docile bacterium that doesn’t die when treated with bog standard antibiotics, or even with some of the more expensive ones that you might be given if you were in hospital with a more serious infection.

Superbugs evolve in the same way that any organism evolves – through the Darwinian process of natural selection, leading to “survival of the fittest”. The difference with bacteria however, is that bacteria don’t just reproduce sexually or asexually like the majority of other organisms – they also have a weird and wonderful way of sharing and swapping genes with other bacterial cells, simply by passing them through the cell membrane as they float past. As well as this, they reproduce so darn quickly – doubling in numbers every few minutes or hours – that natural selection takes place on an accelerated scale. Compare this with the 5 or 10 years that it takes scientists to identify and process new drugs through clinical trials to the open market, and it’s no wonder that our antibiotics are getting out of date.

The thing that’s been getting the scientific community in a tizzy lately is the fact that bacteria carrying a gene that gives antibiotic resistance against a group of antibiotics called carbapenems has been found in the drinking water supplies of the Indian city New Delhi (The Lancet Infectious Diseases (11)70059-7, 2011). The gene, NDM-1, has the ability to transfer into several different bacterial strains, which means that it is likely to spread very quickly, and carbapenems are used to treat the most serious and stubborn, hard-to-treat infections. Thanks to the large amount of international travel to and from India, NDM-1 has already found its way to the UK and healthcare providers are bracing themselves for a crisis.

So what can we do about antibiotic resistance? Well, firstly, we need to stop using antibiotics as a cure-all for the slightest of infections. We humans are just a little bit antibiotic-mad and the fact that Fleming’s wonder-drugs have traditionally been so effective means that we’re happy to pop pills for all manner of small, non-urgent infections, especially in those countries where strong antibiotics can be bought over the counter without a prescription.

Secondly, we need to embrace organic farming and put an end to the practice of feeding our livestock with antibiotics in order to produce bigger and fatter animals for meat. In any battle, if you try the same tactic too many times, the enemy will eventually get wise to it and beat you at your own game. So it is with bacteria. By bombarding our animals with the same varieties of antibiotics over and over again – often needlessly – bacteria are now becoming more and more able to evade our weapons. In fact, a recent study published in BioMed Central’s very own BMC Environmental Health found that flies and cockroaches living in pig poo were an important vector in the transmission of antibiotic resistant bacteria from animals to humans.

Thirdly, we need to stay healthy. Obviously this is easier said than done, but most serious infections with antibiotic resistant bacteria occur in hospitals – not necessarily because hospitals are germ-ridden, but because when we’re in hospital, we’re often immunosuppressed. When our immune systems are weakened, bacteria can take hold and our natural defences are less able to cope, resulting in infections that spread rapidly and can overwhelm us.

Lastly, of course, we need new antibiotics, and new, faster approaches to antibiotic development. A Taiwanese group of researchers have recently published findings in Nature Chemical Biology that demonstrate the potential for tweaking the chemical structure of existing antibiotics in order to improve efficacy. Results have been promising in the Petri dish and rat models, but further tests and trials will need to be done before these drugs can be developed for human use. The question is, will it be too late by then?





The Science Bit – Part 10: Pigs lead the way in Cystic Fibrosis research

1 04 2011

Cystic Fibrosis (CF) is a recessive genetic disorder that affects approximately 8,500 people in the UK. It’s the most common life-shortening inherited disease in the world, with around 1 in 20 people being a carrier for the condition.

CF is caused by a mutation in the gene for a protein called the cystic fibrosis transmembrane conductance regulator or (thankfully) CFTR for short. This protein, in its normal state, is a channel protein that controls the movement of salts from the inside of the cell to the fluid surrounding the cells in the lungs, pancreas and other affected organs. In the sweat glands, CFTR usually works by moving salt from the sweat on the skin back into the body. When CFTR does not work properly however, too much salt and not enough water accumulates in the lungs, pancreas etc, and remains on the skin. The lack of water means that the normally lubricating tissue fluid in these organs becomes thick and sticky mucus.

The most recognisable symptoms of CF are to do with the build up of mucus in the airways, which causes unrelenting, mucusy coughing and a difficulty in breathing. Bacteria thrive on the thickened mucus, so lung infections including pneumonia are common, leading to damage of the airways and general poor health because of the inability to exercise properly to maintain fitness.

Mutated CFTR has effects elsewhere in the body, too. In the intestines, severe, chronic constipation caused by a lack of water to soften stools in the bowel can often lead to infection and rectal prolapse. Food cannot be digested properly in the small intestine, so CF patients often have difficulty in maintaining their weight and growth is stunted. The bile ducts may become blocked and cause damage to the liver. Cystic Fibrosis-related diabetes may occur as a result of the blockage of insulin in the pancreas. 97% of CF men are infertile because of an absence of the vas deferens, the tube that supplies sperm to the penis.

Given all these complications, it’s perhaps not surprising that until only a few decades ago, an infant born with CF would have been lucky to reach its first birthday. Now, although still a relatively short life expectancy, a CF sufferer might live well into their 30s and 40s, and with a successful lung transplant, even longer. Advances in treatment, including respiratory therapy, antibiotics, physiotherapy, diet and lifestyle changes have all made significant improvements to the quality of life for CF patients. But while the symptoms of CF can now be more effectively managed, there is still no cure for the disease.

A key to finding a targeted cure for CF is to understand the genetic and molecular processes that go on at the cellular level. Recently, a team of researchers from the University of Iowa made an important discovery that brings us a little step closer to the end goal of curing this disease. Pigs.

Pigs have long been used as an animal model for human disease research because in many organ systems, they have a very similar anatomy. Of course, there is much about a pig that is different, but by genetically engineering a pig model that mimics the faulty CFTR gene, the research team have been able to discover that the mutated protein has the same pathological effects in their pig model as in humans. This breakthrough means that pigs may now be used in further research to more accurately pinpoint what exactly happens to the mutated CFTR protein, and to find a way to treat it or correct it.

Using their new model, the team, whose findings were published in Science Translational Medicine last week, have already identified that the faulty CFTR protein is “misprocessed” in the cell and ends up in the wrong place, compared to the normal protein. Now that we know that pigs are analogous to humans in the manifestation of CF, they can be used to test a variety of potential new treatments, including gene therapy techniques that replace the faulty gene with a working copy, and “corrector” drugs, which aim to move the faulty protein to its proper position in the cell. The development of a pig model for studying this disease opens new doors to finding a way to beat cystic fibrosis, and new hope to its victims.





BMC Blog VI

18 03 2011

My turn again to moderate the BMC Blog this week – bit of a slow news week at BioMed Central, but here are the blog posts I edited and moderated!





The Science Bit: Part 9 – The Human Genome Project – 10 years on

25 02 2011

The human genome projectIn 2001, the journals Science and Nature simultaneously published the results of a decade or more of groundbreaking scientific research – the Human Genome Project. But what is the Human Genome Project? Why was it done? And most importantly, what have we learnt from it?

Inside almost every one of our cells are chromosomes made up of DNA. DNA is a long, twisted molecule made up of units of 4 chemicals called adenine, thymine, cytosine and guanine and (A, T, C and G respectively), plus some sugar and phosphate molecules to hold it all together. We’ve known for many years that small sections of DNA, called genes, provide the instructions to make different proteins, and proteins are important because they are involved in just about every chemical, mechanical and structural function in the body.

The primary aim of the Human Genome Project (HGP) was to “spell out” the sequences of As, Ts, Cs and Gs for every single human gene. It was hoped that if we can do this and discover what a “normal” gene looks like, then we would also discover the genetic mutations and abnormalities that cause human diseases. Not only that, but by mapping the location of each gene on each chromosome, we might be able to use targeted drug and gene therapy to treat or even cure some of these diseases.

The announcement, in February 2001, that the human genome had been sequenced was front page news. After years of trying, and $3 billion of funding, it had finally been done. Researchers heralded the beginning of a “golden age” for genomic research, and the media were in a frenzy speculating on all the terrible diseases that may now be cured, all the wonderful new drugs that might be developed. But then, after the hype, it all went quiet.

So what has the HGP achieved in the last 10 years? We still haven’t cured cancer, or AIDS, or Alzheimer’s, and stem cell therapy is still a rather experimental treatment for some diseases rather than the miracle cure-all we hoped it would be. Was the HGP a waste of time and money?

Of course the answer to this is “no”. Though, as a result of the HGP, medicine has not advanced as much as we might like in the last decade, our underlying understanding of genomics has made great leaps and bounds. As The Economist’s Science Editor Geoffrey Carr wrote recently, the race (between rival research teams Celera and the International Human Genome Sequencing Consortium) to sequence the human genome “was not a race to the finish line, but a race to the starting line”.

So what have we learned from the HGP? Well, the very fact that the entire human genome – some 3 billion As, Ts, Cs and Gs long – could be sequenced and mapped is in itself a marvellous achievement for scientific research, and the sequencing process has been refined so that it is now much quicker, cheaper and more efficient. Despite humans being one of the most complex organisms on Earth, we’ve learned that the human genome is much smaller than we originally thought – we have around 22,000 genes, in comparison to the very recently-sequenced and very tiny water flea (Daphnia pulex), which has 31,000.

Though the head of pharmaceutical company Novartis once quipped that the HGP had yielded “data, data everywhere, and not a drug, I think”, we are now beginning to see advances in medicine too. While we have not yet witnessed a “revolution” in terms of “the diagnosis, prevention and treatment of most, if not all, human diseases”, as predicted by then-President Bill Clinton in June 2000, we have pinpointed the genetic defects that cause around 850 diseases and this is slowly but surely leading to advances in their treatment. Thanks to HGP research, several new drugs for cancer, osteoporosis and lupus are now beginning to enter the market after a decade of trials, and genetic screening is becoming more widely available for a greater range of diseases.

Despite the deficit in new discoveries that have been sensational enough to rouse the interest of the general public, the Human Genome Project and the ongoing research stemming from it, is still plugging away and helping to increase our overall understanding of genomics. If sequencing the human genome was a sprint to the start line, the race from here on is a marathon, but one that will ultimately impact greatly on biology, medicine and science as a whole.





‘Mum! I’m hungry!’ Hungry chicks have unique calls to their parents

26 01 2011

Scientists studying Jackson’s Golden-Backed Weaver birds have discovered that not only can the parent birds identify their own chicks by the unique sound of their calls, but they can also tell if their chick is hungry, and how hungry.

A press release that I wrote for BioMed Central, following a study published in BMC Ecology, reveals that the more hungry a baby bird is, the more frenetic and unique the call becomes, so that parent birds not only know that they need to gather food for their young, but also how much.

Read the original article at BMC Ecology: The effect of hunger on the acoustic individuality in begging calls of a colonially breeding weaver bird

Read the press release I wrote at EurekAlert: ‘Mum! I’m hungry!’ Hungry chicks have unique calls to their parents

Read some of the press articles that used the press release:








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