Open Access and the Problem of Predatory Publishers

8 02 2015

Last year, I had two scientific papers published in the Journal of Experimental Botany (here, and here, if you’re interested!). For one of these, I was the first author, which was incredibly exciting! Little ol’ me, without so much as a Masters, let alone a PhD, with a publication record! Hurrah!

However, being a published author brings certain annoyances, largely the problem of ‘predatory’ journals.

A librarian chap called Jeffrey Beall has come up with a list of so-called ‘predatory’ journals and publishers – you can find the list here, and a PDF of his selection criteria here. Essentially, unlike ‘proper’ open access publishers, which have rigorous policies and editorial and peer review systems in place, predatory journals will publish just about anything as long as you give them money. They often have bogus editorial boards (or boards made up of people you’ve never heard of), do not peer review manuscripts or have a rigorous process for doing so, and despite many claiming to be based in the US or UK, they all seem to be terribly bad at English spelling and grammar.

In recent months, I’ve had countless emails from companies – without exception all appearing on the Beall’s List – inviting me to submit a manuscript. Given that both of my published papers appear in the Journal of Experimental Botany, I’m not quite sure why these companies feel that I will have anything to offer on the subject of meteorology, or archaeological research, but there you go. Really, they’ve just scraped my email address from J Ex Bot and are trying their luck. It’s very annoying.

A month or so ago, I also had an email inviting me to become an Associate Editor for a predatory journal. Er, what? I used to work for BioMed Central so I know all about the criteria a potential AE needs to fulfil – a strong record of highly cited publications, society or association leadership, extensive experience of being a referee or other senior editorial positions, etc. I don’t want to put myself down here, but it’s fair to say I’m not qualified to be an AE. I have two published papers. Two. No PhD. Plenty of experience of copy editing manuscripts, but none in peer reviewing them. I’ve joined a couple of societies to get cheaper conference registration fees, but I’ve certainly never held a position of responsibility at one. In short, if they want me to be an AE then they’re really scraping the barrel!

Just yesterday, I had yet another badly written email inviting me to submit a manuscript, this time to Global Journal of Science Frontier Research, whatever “science frontier research” is, published by Global Journals, Inc (US) (GJI). Yes, you’ve guessed it, they’re on the Beall’s List. I should have just deleted it, but I was in a mischievous mood, so I replied to “Dr R K Dixit”, stating that I didn’t wish to have anything to do with any publisher on the Beall’s List.

Today, to my surprise, I received a reply – not from Dr Dixit (who, incidentally, is on the Editorial Board of GJI along with two other people with the same surname…hmm…), but from a Steven Mills from the Customer Care department. I won’t republish the whole reply here because it was really long, but it was ridiculous. If it was supposed to persuade me that his was a reputable and legitimate company, it completely failed.

Most of the email made no sense whatsoever, and was written in such appallingly bad English that I almost couldn’t be bothered to decipher it. There was talk of “stumbling rocks” and “funny lists”, extensive inappropriate capitalisation and an inability to correctly use the indefinite article. In one place he referred to “pear review”, and in another “peering reviewing”.

However, in the bits I could understand, he seemed to be giving Jeffrey Beall a right slagging off! Mills accused Beall of being a “mere librarian” of “fully questionable authenticity”, with “limitations” and a “shallow and misguiding” knowledge of research. He accused him of playing “dirty tricks” because he allegedly works for a “mafia” of “Commercial Capitalists”, paid commission by certain big-name publishers to champion their pay-for-access journals over those with an OA model. He even accused Mr Beall of setting up a fake Nigerian mirror of the GJI home page, though quite why he’d want to do that, I have no idea.

Mills attempted to reassure me of GJI’s calibre. “We are pioneer journal publishing house,” he said. “We have rigid quality control mandatory procedures viz. Peer Review and Plagiarism Check. We are having highly qualified team of approximate 1200 nos. pear reviewers.”

Um, yeah, not convincing me, Mills…

“We are registered organization at Delaware (USA) [but their US address is in Massachusetts?] and affiliated to Open Association of Research Society (USA).”

I googled the Open Association of Research Society (the name of which totally doesn’t make sense, by the way!). This organisation is allegedly registered in Delaware, but its website is riddled with exactly the same kinds of spelling and grammar errors as the GJI website – oh, and they have really similar logos… Who else thinks GJI made it up?!

After his long tirade of abuse and waffle, “Steven” closed by thanking me for bringing this “serious conspiracy” to his attention and vowed to take “suitable stringent legal actions against Mr Beall for showing our name in his list of fake journals mischievously if he does not apologize publicly and withdraw his allegation”.

Yeah…good luck with that.

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Scientific copyeditor at your service

9 10 2014

Wow, I haven’t posted on this site for a LONG time. Sorry about that, I’ve been very busy as usual! But I have something for you today that I wanted to share…

In the course of my day job at the University of Warwick, I compile a weekly ‘Arabidopsis Research Round-up‘ of recently published, UK-based scientific articles in the area of Arabidopsis research. (FYI: Arabidopsis thaliana is a small weed used as a model organism for plant research – you can find out more about it here: http://youtu.be/hWAb30Ggl5o.) This involves reading lots of abstracts of new papers and condensing them into easy-to-read summaries, which we then publish on the GARNet website, blog, and on the Arabidopsis Information Portal.

Today’s Round-up will include this article, led by a Chinese team but also involving a British scientist from Rothamsted Research: Yang L, Zhao X, Paul M, Zhu H, Zu Y and Tang Z (2014). Exogenous Trehalose Largely Alleviates Ionic Unbalance, ROS Burst and PCD Occurrence Induced by High Salinity in Arabidopsis SeedlingsFrontiers in Plant Science, DOI: 10.3389/fpls.2014.00570.

As someone without extensive lab experience, it’s not unusual for me to sometimes get a little stuck when reading complex scientific papers. But, with a a little effort, and the help of Google, I’m pretty good at unpicking the terminology to work out what the paper is really about so I can translate it into plain English. This paper, however, took a little more unpicking than most; in fact, the abstract didn’t even make sense in places!

Here is my copyedited version of the manuscript’s abstract:

Although Ttrehalose (Tre) has been reported to play a critical role in plant response to salinity, and the involved mechanisms remain involved have yet to be investigated in detail. Here, the putative roles of Tre in the regulation of ionic balance, cellular redox state, and cell death were studied in Arabidopsis under high salt conditions. Our results found that the salt-induced restrictions on both vegetative and reproductive growth in salt-stressed plants were largely alleviated by an exogenous supply with of Tre. The mMicroprobe analysis of ionic dynamics in the leaf and stem of inflorescence stem highlighted the Tre‘s ability to retain the K and K/Na ratio in plant tissues to improve salt tolerance. The In flow cytometric (FCM) assays of cellular levels of ROS (reactive oxygen species (ROS) and PCD (programmed cell death (PCD), displayed that Tre was able to antagonized salt-induced damages in both the redox state and in cell death. and sSucrose did not play the same role with Trewas not shown to have the same effect. By cComparing ionic distribution in between the leaf and IS (inflorescence stem (IS), we found that Tre largely improved was able to restrict Na transportation to IS from leaves since that the ratio of Na accumulation in leaves relative to IS. was largely improved due to This shows that Tre was able to restrict Na transportation to IS from leaves. The marked decrease of Na ions, and the improved sucrose levels in IS, might account for the promoted floral growth observed when Tre was added to the saline solution. At the same time, endogenous soluble sugars and the activity of antioxidant enzymes activities in the salt-stressed plants were also elevated by Tre to counteract high salt stress. We concluded that Tre could improve Arabidopsis salt resistance with respect to biomass accumulation and floral transition in the by means of regulating plant redox state, cell death, and ionic distribution.

I contacted Frontiers in Plant Science about this via Twitter, and they assured me that this is a provisionally accepted manuscript that has not yet gone through the copyediting and typesetting process. Still, if I’d been reviewing this manuscript, I think I’d have pushed for a pre-acceptance copyedit – especially as one one of the authors on this paper is English himself!

I would always recommend authors to have a native English speaker read through and comment on a manuscript before submission – even if the author him or herself is also a native English speaker. Of course, I would love that editor to be me (contact me for copyediting and proofreading at a very competitive price!) but it could just be a friend or colleague who has not worked on the document.

Minor mistakes such as inconsistent formatting or mixed use of British and American English can be ironed out by the publisher’s in house team (if they offer this service – not all do!), but, in my opinion, it just doesn’t make sense to submit something that doesn’t make complete sense or which is full of errors. As an author seeking to have your work published, you’ll want to make the review process as easy as possible for the editors and reviewers. Not only will this speed up the process, but it could make the difference between getting published in a low impact journal when you were aiming for a higher impact one, or even getting published at all.

Perhaps I am being pedantic and impatient with the publication process – what do you think?

 

 





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





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!








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