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.

Anyway, back to the subject of this blog post.

If you’re a Facebook user, you’ll notice that the adverts that appear on your pages are quite often cleverly targeted to whatever you have been writing about on your Wall. Over the last few weeks, I’ve attended two hen parties and was a bridesmaid at my friend’s wedding, so of course the ads on my Facebook page have been all related to rings, dresses, cakes and wedding photography. Then, just yesterday, a friend posted, “Health kick has begun! 15K run and only one chocolate bar consumed today!” Ever since I congratulated her on her efforts, I’ve had sports and dieting-relating ads appear on Facebook – and it’s one of those ads that I want to talk about today because it’s got me rather riled!

The offending advert is this one; “Cheryl Cole Loses 19lbs”. Even without clicking the link, the advert has got me mad – Cheryl Cole is TINYand I rather suspect that the advert text is not only misleading but also factually incorrect. Intrigued, I decided to click the link in the advert, and was directed to a NOW Magazine article that discusses how between them, the 5 members of British girl band Girls Aloud allegedly lost 36lbs in weight. Weirdly, the article doesn’t mention “these 2 old diet tips” proffered in the advert, though the page is loaded with miracle diet-related Google ads, and even more oddly, the NOW article was from 2006!

Immediately getting on my soapbox, I wrote to NOW Magazine and pointed out the many inaccuracies and misleading titbits quoted in the article.  For starters, the Facebook ad claims that our Cheryl lost 19lbs in weight; the NOW article says she lost 14lbs. More seriously, I felt that NOW Magazine were glamourising Cheryl and her bandmates’ unnecessary weight loss (and it is at this point that I should point out I don’t know if the figures quoted are even true or not!). According to the article, 5 ft 3 in Cheryl has gone from 9 stone to 8 stone, and suggests that the higher weight was unhealthy. In fact, for Cheryl’s height, both 9 stone and 8 stone are well within the “healthy” Body Mass Index (BMI) bracket.

Even more worrying were the weight loss figures quoted for her bandmates Sarah Harding and Nadine Coyle, both of whom have reportedly lost 7lbs. However, at 5 ft 6 in and 5 ft 5 in respectively, both Sarah and Nadine’s starting weights were at the lower end of the “healthy” BMI bracket, and their alleged weight loss has now put them in the “underweight” category. Despite this, Nadine Coyle is reported as saying that she still feels she has “curves” – which we all know is magazine-speak for “fat”. This is not something that I feel a woman’s magazine should be promoting!

Though it is 5 years old, I am shocked and appalled that this article was even published in the first place. Many people, especially young girls, look up to Cheryl Cole and the other members of Girls Aloud, and it’s easy to see how these impressionable groups could be led to believe that 8 stone or less is “the perfect weight”, especially in the absence of any explanation of the Body Mass Index – a measure of how your weight is relative to your height. The article also fails to mention that many secondary factors can be attributed to weight – genetics, metabolism, muscle to fat ratios and gender, among other things, can all affect your weight and alter what an individual’s ideal weight should be.

The thing that angered me most about the article was not even the article itself, but rather the way in which I was made aware of the it – through a targeted Facebook advert that was presented to me on the grounds that I congratulated my friend Jenny on her running achievement and chocolate-avoiding will power. It appeared to me to be part of some highly unethical pay-per-click marketing campaign in which young Cheryl Cole fans would see the ad and think, “OMG! If Cheryl Cole needed to lose 19lbs then what does that mean for me?! What can I do about it?! Oh look, there seems to be a Google advert, conveniently placed directly underneath this article, that promotes a miracle diet cure! I’d better try it!” And just like that, NOW Magazine earns a few pence from the ad click, and another teenage girl becomes deluded – or anorexic, eating only rocket salad and balsamic vinegar, just like Kimberley Walsh.

But there’s a twist in this tale! I immediately fired off a complaint email to NOW Magazine and was surprised when, not less than a few hours later, I received a reply that said,

From: Now online
Sent: 10 May 2011 16:34
To: Lisa Martin
Subject: Re: Complaint about Facebook ad article link

Dear Lisa Martin
We do not have any Facebook ads and this article, as you say, is 6 years old so we are perplexed by your letter.

What Facebook ads please? Do you have a grab of one?

So I sent a screen grab and replied,

Hi,

Well I’m somewhat comforted to learn that you don’t seem to know anything about this Facebook advert (though I still think the article is terribly written, even if it is 5 or 6 years old!), but please find attached a screen grab of my Facebook homepage (as of 5pm today) with the offending “ad” on the right hand side. The link directs to your article at http://www.nowmagazine.co.uk/celebrity-profiles/diets/230337/girls-aloud-s-diet-secrets/1/.

Would appreciate an update!

Thanks,

Lisa

NOW Magazine sent a brief reply saying, “Will let you know. This is very odd”.

Very odd indeed! What’s going on here?!

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?

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.

I’m planning some changes here on my blog and I’m just writing to let you know that you might experience some disruption while visiting lisaamartin.wordpress.com over the next week or so.

Thanks to the huge success of my posts about Freelancer.com and freelancing in general, the focus of my blog has diverged somewhat. It originally started as a place for me to showcase my freelance portfolio, and as a place where people who wanted to hire me could find me online. I still want to maintain both my general freelancing and portfolio posts, but I think the time has come to separate these two quite different aims into two blogs.

Because the URL to this blog is on all my business cards, stationery and contracts, lisaamartin.wordpress.com will become my portfolio blog. It’s kind of annoying to have to do it that way around, since a lot of my traffic comes from the general freelancing posts, but since the majority of that traffic comes from random searches, I hope that the new blog will quickly build it’s own traffic. The new blog, by the way, will eventually be at freelancerlisa.wordpress.com. There’s not much to see there yet, but if you’re a subscriber to this site for my posts about freelancing, I suggest you head over there and sign up for emails to make sure you’re kept in loop about the forthcoming changes and eventual switchover!

If anyone has an idea for a better name for my new freelancing blog, please comment with your ideas!

• Translational stem cell genomics
• Arthritis Research & Therapy’s new look
• Journal of Nanobiotechnology tracked by Thomson-Reuters
• Guidelines to improve the reporting of genetic risk prediction studies

I recently completed my first project in British pounds, but hit a stumbling block when I tried to withdraw the funds from my Freelancer account to PayPal. I had £45 in my account, but when I requested to withdraw £45, an error message flashed up on screen saying, “ERRORS OCCURED – Withdrawal amount cannot be more than overall balance”. Huh?

Although Freelancer takes a £1 fee for PayPal withdrawals, this is usually deducted after you have requested the balance, i.e. you request to withdraw £45 and you receive £44 in your PayPal account. If I entered an amount of £44, this was accepted, but after the £1 fee, this would leave me with an amount of £1 in my account.That’s my pound! I want it!

I queried this situation with Freelancer Support and for once I received a straight answer! Helpful Shane said, “It appears that there is a bug in our system caused by the rounding of fees.” To remedy this situation, Helpful Shane deposited 1p into my account, making my balance £45.01, which has now allowed me to withdraw the full £45 that I earned. Hurrah!

I’m not sure if this happens if you try to request a withdrawal in other currencies, or if the same thing happens if you use Moneybookers or another withdrawal method, but if you’ve experienced the same thing, please leave a comment here to help and advise others. If this happens to you, contact Freelancer Support (customer-support@freelancer.com) and they will be able to help you. An engineering team are allegedly working to fix this problem so hopefully it won’t be an issue for too much longer.

method5 wanted fresh copy for their clean, new site and to “get the message across” simply, without too much jargon, and in a cool, quirky style. I’ve mixed bold type and catchy headers with friendly-sounding, informative text that doesn’t take itself too seriously, yet still shows that method5 know what they’re talking about. Since I couldn’t get the phrase, “there’s method in our madness” out of my head while writing this site, I’ve thrown in a few Madness song titles too. I’m not sure if Canadians are that big into two-tone, but method5 seemed to like it!

In 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.

First of all, the public message boards. Each project description page, say for instance, this one, has a link to a “project clarification board” – that’s the proper name for the public message board, and it’s an important name. This message board is where you’re supposed to ask questions to clarify details about the project before you place a bid. In theory, the buyer is supposed to read the comments on this message board and answer any questions that potential bidders might have so that they can make an informed decision about whether or not they want to bid, and if so, how much to bid. That’s it. That’s all this board is for.

Here’s what the clarification board (public message board) is NOT for:

• Placing a bid. Bids MUST be placed via the proper bid form (the blue button on the other side of the page, where it says “Bid on this project”). If you place a bid on this message board, you’re breaking terms and conditions and could be suspended. Regular freelancer members have a finite number of bids that they can make per month, so this rule is to stop people who have spent their bids from trying to get an extra chance or ten (TIP: if you find yourself running out of bids each month, upgrade to Gold membership – you’ll get unlimited bids for a monthly fee). Also please note that there is a minimum bid amount of $30. You cannot bid lower than that, so bidding on the public message board is not a good way to get around this!
• Uploading your samples. I actually don’t really know why there is the facility to upload files to the public message board – I don’t see any need for it and it can actually be damaging for freelancers to do so. People who post samples here should realise that because the board is public, ANYONE can access and download those files. ANYONE. Even people who are not registered Freelancer users. Even people who might collect samples and republish them elsewhere without your permission. Even (*gasp!*) buyers who might take your work without asking and not pay for it!
• Uploading your CV (résumé). As above, remember that ANYONE can view files that are posted to the public message boards, so if your résumé contains your email address, your date or birth, your home address, etc etc, these all have the potential to be collected and abused by less scrupulous folk. This also breaks the next rule about…
• Posting your contact details. I’ve said it before and I’ll say it again – it is against Freelancer’s rules to post your contact information ANYWHERE on the site, other than when you first register for an account. Contact information includes your email address, phone number, home address, instant messenger ID or any other way that someone might be able to contact you other than through the Freelancer site. It even includes not-so-cunningly disguised email addresses such as “name at domain dot com”. The reason? Freelancer have been clever enough and kind enough to provide the infrastructure for you to find work by hooking you up with employers. If you contact them outside of Freelancer, you dodge having to pay Freelancer’s commission fees if you win a project. Like it or not, Freelancer, as a business, are entitled to make money, just like you, so pay the darn commission fees and bid/accept bids properly! If you don’t, well then don’t be surprised if your account is suspended, much like the idiot featured in this Freelancer blog post.
• Posting a project or advertising another website. I’ve seen this quite a lot lately. Buyers who don’t want to play by the rules or pay Freelancer’s fees, instead try advertising a project on the public message board. This not is not only a deliberate attempt to dodge fees, but these users usually have to leave a contact email address or IM ID to get people to respond, so that’s two counts of Freelancer felony! I’ve also seen people advertising their companies, their affiliate schemes or other freelance websites here. It’s not allowed!

Each project also has an associated private message board. This is ONLY available to people who have placed a bid using the designated bid form – you cannot send a private message to a buyer until you have placed a bid. On the bid form, right at the bottom, you will find a little check box that says “Also send a private message to the project seller”. Check this, and a message box will appear and you can tap out your message to the buyer. The message will only be sent when you confirm your bid. If you chose not to send a private message at the time of bidding, you can still do so later by accessing the project from your project table (Projects > My Projects). Thereafter, you can message the buyer in private to your heart’s content.

As with the public clarification board, you are NOT allowed to post your contact details on the private message board! The private message board is “private” in the sense that the message cannot be viewed by Freelancer users other than yourself and the buyer, but it does not mean that Freelancer staff cannot see it! If you post your contact details here, or try to bypass any other rules and regulations, Freelancer have access to all this information – they can and will use it as evidence to suspend your account, just like the guy in the Freelancer blog post I mentioned earlier.

By all means, if you trust the buyer, feel free to post your samples and your résumés on the private message board (but be careful to remove any contact information first) and continue to discuss the project. Remember that even if a buyer replies to your private message, even if they show interest in hiring you, hell even if they SAY they want to hire you – the project is not yours until you have received that all-important congratulations email from Freelancer.com asking you to accept or reject the project AND until you have actually accepted it!

As the saying goes, “to be forewarned is to be forearmed”. I’ve told you everything you need to know about the Freelancer message boards – now make sure you get it right!