Can I please buy one of your kidneys?

Should we legalise the sale of human organs?

In the UK alone the average waiting time for a kidney transplant is 3 years, this costs the NHS around £24,000 per patient per year and in 2013 – 2014 1000 people died whilst on the transplant waiting list. Dialysis patients also often say they feel that they are just existing rather than living. But, if these patients could get a transplant from a living donor, their life expectancy would increase up to 23 years and their lives could really begin. With increasing cuts to the NHS budget is it possible that the cost-effectiveness of kidney transplant might persuade the government to legalise a market in human organs?  The implementation of a legal organ market would also increase the human organ supply and eliminate the consequences of the black market.

Due to a shortage in organs, the black market and transplant tourism is thriving. Annually, 15,000 – 20,000 illegal kidney transplants take place around the world, often in developing countries such as India and the Philippines. There are even slums in the Philippines dubbed “kidney-vile”, as the majority of the slum’s residents have been driven to sell a kidney. But the black market is built on systematic deception. Brokers coerce desperate workers to sell a kidney then give them much less money than they were promised. Nor do they care about the surgical quality and often leave donors with little or no aftercare. Consequently, donors often become ill and are unable to continue their usual hard labour, which perpetuates their poverty, rather than alleviating it. Recipients are also affected by black market fraud: often these kidneys are not screened properly and donors are coerced to cheat their medical records. As a result of these schemes and poor hygiene standards, recipients often contract diseases such as hepatitis B/C and HIV.

Group of men from Baseco “Kidney-ville” in Philippines, displaying their scars from selling a kidney.

Group of men from Baseco “Kidney-ville” in Philippines, displaying their scars from selling a kidney.

Iran is currently the only country with a compensated and regulated kidney donation program. In this system, there are no brokers and it is charity organizations that coordinates donors with recipients. The government pay a fixed price for organs and cover the costs of all necessary aftercare for donors. Due to this system, Iran is currently the only country with no kidney transplant waiting list. It has also successfully eliminated its black market, and has still maintained a respectable percentage of altruistic donations. Nevertheless there are flaws to the Iranian system as discussed here.

Erin & Harris proposed an ethical, highly regulated, system in which only individuals within a nation are eligible to sell or receive organs. The market would have one purchaser (e.g. the NHS in the UK) and organs would be allocated fairly, giving recipients an equal chance of receiving a transplant regardless of their economic background. This system would also remove the draw for brokers, and subsequently reduce the exploitation of vulnerable people. Medical screening would ensure only healthy individuals could sell an organ, which would to minimise risk (Gill & Sade, 2002). Such a system would also provide proper medical care for donors who would also benefit from a full psychological evaluation, to make sure they are aware of the consequences of their actions.

A study of 478 donors from the Iranian regulated system has shown their health did not deteriorate after the sale, and that 90% of them were content with selling their kidney. These results contrast markedly with the study of 305 Indian donors in an unregulated market. The health of 90% of these donors declined, people living below the poverty line rose up to 20% and 79% of donors would not recommend selling a kidney. This shows that within a regulated program, both vendors and patients are better cared for and are more satisfied with the transplant process.

The strongest argument against the sale of organ is the possible exploitation of the poor. Critics argue that legalisation could lead to a market that would exploit poorer people, as they might view organ sale as a last resort. But, is it exploitation if a person makes a reasoned decision to take an action they consider to be the best option to improve their life? One can’t assume that money would simply overrule a person’s judgment. A black market would also lead to greater exploitation than any legalised market ever would. Prohibiting an organ market is paradoxical, to restrict an individual’s autonomy and cause moral harms to liberty.

Another prominent argument against the sale of human organs is that it would lead to commodification of the human and therefore corrupt human dignity. Commodification is an unsuitable term to use for the sale of a kidney, since there are numerous other circumstances when paying money does not insinuate loss of dignity, such as surrogacy.The scarcity of organs and, death and exploitation of people will not be resolved through rhetoric of moral repugnancy and human dignity.

Under prohibition, patients are suffering and dying whilst waiting for a transplant. Both vendors and recipients are exploited by the black market, and the human rights of poor people are violated. These problems will continue to exist as long as there is a dearth of organs. So, should a market in human organs from living persons be legalised? Or is it merely a naive and impractical idea, only appropriate for a dystopian future. Either way, the possibility of legalising a regulated and ethical market should be explored.

Post by: Alyssa Vongapai


References

Erin, C. A., & Harris, J. (2003). An ethical market in human organs. Journal of Medical Ethics , 29 (3), 137–138.

Ghods, A. J. (2009). Ethical issues and living unrelated donor kidney transplantation. Iranian Journal of Kidney Diseases , 3 (4), 183–191.

Goyal, M. (2002). Economic and Health Consequences of Selling a Kidney in India. Journal of the American Medical Association , 288 (13), 1589.

Higgins, R., West, N., Fletcher, S., Stein, A., Lam, F., & Kashi, H. (2003). Kidney transplantation in patients travelling from the UK to India or Pakistan. Nephrology Dialysis Transplantation , 18 (4), 851–852.

Hippen, B. E. (2005). In defense of a regulated market in kidneys from living vendors. The Journal of Medicine and Philosophy , 30 (6), 593–626.

Kidney Org. (2010). Transplantation Cost Effectiveness. [Online] Available from:http://www.kidney.org.uk/archives/news-archive-2/campaigns-transplantation-trans-cost-effect/. [Accessed on 5 Aug 2016]

MacKellar, C. (2014). Human Organ Markets and Inherent Human Dignity. The New Bioethics: A Multidisciplinary Journal of Biotechnology and the Body , 20 (1), 53–71.

Moazam, F. (2009). Conversations with Kidney Vendors in Pakistan. Hastings Center Report, (June), 29–44.

New Internationalist. (2014). Human traffic: exposing the brutal organ trade. [Online] Available
from:http://newint.org/features/2014/05/01/organ-trafficking-keynote/. [Accessed on 5 Aug 2016]

Organ Donation. (2015). Transplant save lives. [Online] Available from:http://www.organdonation.nhs.uk/newsroom/fact_sheets/transplants_save_lives.asp.
[Accessed on 5 Aug 2016]

Pat Roque. (1999). Group of men from Baseco “Kidney-ville” in Philippines, displaying their scars from selling a kidney [Photograph]. At: https://digital.newint.com.au/issues/88/articles/1890. [Accessed on 5 Aug 2016]

The Wall Street Journal. (2015). Cash for kidneys: The case for a Market for organs. [Online] Available from:http://www.wsj.com/articles/SB10001424052702304149404579322560004817176.
[Accessed on 5 Aug 2016]

World Socialist Web Site. (2015). Dramatic increase in worldwide illegal organ trade. [Online]
Available from:http://www.wsws.org/en/articles/2012/07/orga-j14.html. [Accessed on 5 Aug 2016]

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Insight from behind the lab bench: Could a period pain treatment be re-purposed to treat Alzheimer’s disease?

Today we are lucky enough to have the opportunity to publish a post written by Mike Daniels – one of the researchers behind the recent discovery that a drug used for the treatment of period pain may have a role to play in the treatment of Alzheimer’s disease. We hope you enjoy the opportunity to slip behind the lab bench and see what happens behind the scenes of a big scientific discovery.

My name is Mike Daniels, I am a PhD student working at the University of Manchester. We’ve just published a paper in the journal Nature Communications on how currently available drugs may be used to treat Alzheimer’s disease. The Brain Bank North West got in touch with us and gave us a fantastic opportunity to add our voice to the current media storm surrounding this research. I hope I can give you a detailed look at the ins and outs of this important research and offer some insight into the workings of a big research project.

Screen Shot 2016-08-19 at 20.48.07Our lab group are particularly interested in AD, not just because it affects over 26 million people worldwide without any truly effective treatment but also because our speciality is immunology and research suggests that an overactive immune system may play an important role in AD. One particular part of that immune system recently implicated in AD is something called an inflammasome. The inflammasome is a large bundle of proteins which forms a kind of machine within cells whose job it is to produce proinflammatory cytokines. These cytokines go on to promote inflammation in the brain which can worsen AD.

What’s particularly exciting for us is that this inflammasome appears to be largely redundant in everyday immune functions like fighting bacteria or viruses. This means we should be able to inhibit it in patients without rendering them susceptible to infection.

OK so we have a plan – inhibit the inflammasome complex in the hope of improving outcomes for people living with AD. But how do we do this? We could design new drugs (something our lab is involved in right now) but the process of getting a new drug from bench to clinic can take around 20 years and cost around 1.6 billion dollars. Another quicker, cheaper option is to do something called ‘repurposing’, this basically means taking a drug already approved and on the market and using it to treat a different disease. With this in mind our lab head Dr. David Brough decided to test a number of drugs from a large class called non-steroidal anti-inflammatory drugs (NSAIDs) to see if they could inhibit the inflammasome and thus potentially be used in AD. So, this was the project I was tasked with in my first week of PhD life nearly two years ago.

We began by testing a number of these NSAIDs on immune cells cultured in a petri dish. This gave us the important opportunity to screen a large number of drugs without unnecessary use of animals. When we ran these screens we had a bit of a surprise. The more famous NSAIDs such as ibuprofen (Nurofen) had no effect. However, one drug, mefenamic acid, was able to inhibit the inflammasome and prevent release of inflammatory cytokines in the cells. Mefenamic acid is only available by prescription and is prescribed largely to treat period pain.

So, how does mefenamic acid inhibit the inflammasome?

Research suggests that ion channels on the cell surface play an important role in inflammasome activation and that mefenamic acid may inhibit some types of ion channels. To better understand this we formed a collaboration with a London-based research group led by Dr. Claudia Eder – an expert in electrophysiology (researching ion channels). It was with the help of Dr. Eder’s lab that we identified the target of the drugs as a chloride channel called the volume-regulated anion channel (VRAC).

Screen Shot 2016-08-19 at 20.56.56Now we had the drug and the mechanism but we still don’t know whether this drug would be effective in treating AD. This is where we needed to look at the drugs action in a living system. The first model system we chose was a rat model of amyloid-beta induced memory deficits. Build-up of amyloid-beta is a thought to be a major factor in memory impairment and AD. Indeed, if injected into the brain of rats, amyloid-beta causes permanent memory deficits. As part of a collaboration with Dr. Mike Harte’s lab here at Manchester, we injected a group of rats with either mefenamic acid or a placebo and found that those which received the drug were completely protected from amyloid induced memory deficits.

We then moved to look at the effect of the drug in a genetic mouse model of AD. These mice had been altered to express some of the same genes found in humans with the genetic form of AD and, like human sufferers, these mice develop memory deficits with advancing age. When treated with mefenamic acid at the age of onset, these mice did not develop memory deficits, unlike animals treated with a placebo. We also found that the brains of placebo mice displayed signs of intense inflammation while those of drug treated mice remained completely normal.

So to conclude, AD is a terrible and currently incurable disease which we believe to be partially caused by an overactive immune system – specifically over-activity of a protein complex called an inflammasome. We found that the commercially available drug mefenamic acid was able to inhibit the inflammasome and reduce memory loss in both mouse and rat models of Alzheimer’s-like memory deficits.

But what’s the next step? We are hoping to begin to move mefenamic acid into clinical trials to see if it could really work in humans. Luckily, because the drug is already known and approved we can skip the safety testing stage of the clinical trial process. Unfortunately however, clinical trials remain extremely expensive and, as mefenamic is off patent and can no longer be sold for profit, gaining funding through pharmaceutical companies is nigh-on impossible. This means we are relying on grants from fantastic charities such as Alzheimer’s Society and Alzheimer’s Research UK in order to move this study forward.

A lot of work is needed and it will still be a while before we have results in people currently living with AD, but this remains an exciting step and we can only hope that it will go some way to treating this horrible disease.

Guest post by: Mike Daniels

Screen Shot 2016-08-19 at 20.25.13Mike is currently studying for a PhD in neuroinflammation at the the University of Manchester, UK. His work is based mainly on the role of a huge protein complex called the inflammasome in diseases such as Alzheimer’s, stroke and haemorrhagic fever. When he’s not in the lab he’s usually found up a mountain or out in the countryside somewhere and is always on the lookout for any new science outreach ideas!

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Fat vs fat in the fight against obesity and diabetes

Using fat to treat obesity and obesity-related conditions, such as type II diabetes, may sound like a strange idea. Nevertheless, this is exactly what scientists are working to achieve. So the question is, why?

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There are in fact two types of fat in the body. The more familiar of the two – white adipose tissue (WAT) – is the tissue we refer to colloquially as “fat” and associate with gaining weight. The second, and lesser known variety of fat, is brown adipose tissue (BAT). This unique tissue is densely innervated by the body’s sympathetic nervous system (SNS – initiator of the “fight or flight” response) and is well supplied by blood vessels. Originally believed only to exist in small mammals and human infants. BAT is used to produce heat without the need for shivering. This is particularly important for these organisms as a way of maintaining their core temperature in mild cold conditions.

The key to BAT’s ability to produce heat is a special protein called uncoupling protein 1 (UCP1), which is housed within the large number of mitochondria found in this tissue. In general, mitochondria act as the “powerhouses” of all cells, producing energy in the form of ATP which allows the cell to perform all its required functions.

However, in cold conditions, sensors on the skin send a signal to the part of the brain responsible for regulating body temperature. The brain, in turn, sends a message to BAT via the SNS, releasing noradrenaline and stimulating UCP1. Upon activation, UCP1 is able to “override” the usual ATP-synthesising function of BAT mitochondria, instead releasing energy as heat.

Importantly, this process of heat production requires a significant amount of energy to achieve. As the main fuel used by BAT are fat molecules, such as lipids and fatty acids, the idea that BAT could potentially be used to help reduce body weight in obesity is not as ludicrous as it may first appear. This is supported by the finding that both UCP1- and BAT-deficient mice models display increased weight gain.

Screen Shot 2016-08-14 at 20.48.58Despite evidence of the role BAT plays in controlling body weight in experimental rodent models, BAT was originally believed to be absent in adult humans. More recently, however, the use of radioactive tracer PET and CT scans have demonstrated the presence of functional BAT in adults in mild cold conditions using large cohorts of patients. Further analysis of PET and CT data has also uncovered an inverse association between BAT activity and BMI, with lower levels of activity in patients with severe obesity. Though the average human adult is estimated to possess just 50–80g of BAT, this mass is believed to use up to 20% of our daily energy intake, making BAT a desirable candidate to aid weight loss in obesity.

BAT has also been shown to express high levels of the glucose-transporter protein and displays comparable glucose uptake to muscle in response to insulin. Given that a key risk factor for type II diabetes is being overweight, and that this disorder is characterised by high blood glucose and insulin resistance, targeting BAT as a method of treatment is also under investigation. Notably, insulin-activated glucose uptake into BAT is significantly lower in those with obesity compared to subjects of a normal weight.

Given the mechanism of BAT activation discussed above, as well as the observation during PET and CT scans that BAT activity is inhibited when human subjects are warmed, the simplest way to stimulate this tissue for therapeutic reasons may be with the use of cold temperatures. In support of this theory, a small study involving healthy Japanese volunteers, who were repeatedly exposure to mild cold stimuli over 6 weeks, reported increased BAT and resulted in a loss of body fat in subjects. In another study, exposing healthy volunteers with active BAT to short-term mild cold led to increased insulin sensitivity.

Screen Shot 2016-08-14 at 20.49.22A second potential method of stimulating BAT with the aim to treat obesity or type II diabetes is via the SNS, specifically through beta-adrenergic receptors (βARs). It should be noted that anti-obesity medications which target these receptors have been tested in the past. However, these attempts failed due to unspecific activation of βARs throughout the body – particularly the heart – resulting in serious side effects, including increased blood pressure and heart rate. Nevertheless, the use of more specific βAR agonists have been used successfully to increase BAT activity and lessen obesity and insulin resistance in rodent models, without such side effects.

Alternatively, it may be possible to target the thermoreceptors on the skin responsible for sensing cold, known as TRPs. As cold exposure cannot be controlled easily, activating these receptors artificially may provide a more efficient way of using BAT to treat obesity or type II diabetes. Interestingly, there are already a number of foods which activate TRPs, including menthol in mint and capsaicin in chili peppers. Animal and human studies of capsinoids – non-pungent analogues of capsaicin – have demonstrated that these compounds increase active BAT and reduce body fat.

Despite sounding rather contradictory, adipose tissue may prove useful in the treatment of obesity and the obesity-related disorder, type II diabetes. Unlike its white counterpart, BAT actually uses up lipids and glucose from the body as fuel in order to produce heat. However, in doing so, evidence suggests this can also result in weight loss, reduced insulin resistance and lowered blood glucose, making it a potential treatment for obesity and type II diabetes. Possible methods of activating BAT for this purpose may include cold stimuli or agonists which target βAR or TRP receptors. It is still early days for this treatment possibility but the idea certainly isn’t as strange as it may first appear.

Post by: Megan Barrett

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Rheumatoid arthritis and Alzheimer’s disease, what’s the connection?

It has recently been reported that a drug currently used to treat rheumatoid arthritis (RA) may also pack a punch in the fight against Alzheimer’s disease (AD). This discovery may be hailed by the media as a big step forward for AD research but what does it really mean?

To pick apart this discovery, we first need to delve into some background on Alzheimer’s itself:

Screen Shot 2016-08-08 at 20.47.27Much of what we know about Alzheimer’s disease in the human brain comes from postmortem studies. This means that most of our knowledge is skewed towards late stages of the disease. We know that, in these late stages, patient’s brains are severely shrunken and littered with clusters of abnormal proteins known as amyloid plaques and tau tangles. Many academics acknowledge that if we want to successfully treat AD it’s important that we understand what causes these proteins to misbehave in the first place. This is where scientists picked up on an important link between RA and AD.

Rheumatoid arthritis is an autoimmune disease which causes inflammation, pain and swelling in joints. Interestingly, alongside chronic inflammation, many RA sufferers also experience what is known as secondary amyloidosis resulting from deposition of amyloid protein fibrils. This form of amyloid starts life in the liver before being cut into smaller pieces and then deposited in other tissues – importantly this process appears to parallel the deposition of amyloid in the AD brain. Another important parallel between the two diseases is the presence of tumor necrosis factor (TNF) – a pro-inflammatory cytokine. Researchers believe that RA may be driven by TNF and it is also known that AD patients show elevated levels of TNF in their cerebrospinal fluid.

So, is it possible that TNF could play a causative role in both RA and AD and, if so, can modulation of TNF be used as a treatment for both diseases?

In a recent study Richard C.Chou from Dartmouth-Hitchcock Medical Centre collected medical records from over 8,000,000 US patients and his team began crunching numbers in the hope of answering these questions. They found that patients suffering from RA (over 40,000 patients) had a significantly increased risk of also developing AD. In fact, RA patients over the age of 65 were more than twice as likely to suffer from AD than non-sufferers (2.95% of RA patients also suffered from AD in comparison to 1.37% of non-RA patients). What was even more interesting was that patients treated with the RA drug etanercept (an anti-TNF agent) were significantly less likely to suffer from AD than other RA patients.

These results suggest that both RA and AD may share a common mechanism, perhaps linked by the actions of TNF? It also raises the possibility that anti-TNF therapies could have a future in the treatment of AD.

Although this work is just one more piece in the Alzheimer’s puzzle, the implications seem to suggest a role for inflammation and perhaps TNF in disease progression – something which has also been highlighted in previous studies. So, although (as is often the case) more research is needed, it does seem like we are making some significant headway in understudying and hopefully treating Alzheimer’s.

Post by: Sarah Fox

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Why do astrophotographers spend all night under the stars?

It’s a sensible question. You may think that our love of the celestial domain keeps astrophotographers up all night, or maybe it’s because there are so many astronomical targets out there that it takes all night to photograph them. Or maybe because our telescopes are so complicated and delicate it takes us hours to set them up. Well these points may partly explain why I frequently keep my wife awake as I struggle to move my telescope back into the house…often past 4:00am! But there is a deeper reason; one that means almost every astronomical photo you see probably took hours or days of photography to produce. In this post I shall explain, with examples, why I and other poor souls go through this hassle.

Let me begin by saying that during a single night (comprising maybe 4-6 hours of photography time), I certainly do not spend my time sweeping across the night sky snapping hundreds of objects. Instead, I usually concentrate on photographing  1 or 2 astronomical targets – taking more than 40 identical shots of each. In this regard, astrophotography is quite different from other forms of photography. But why do this, what is the benefit of taking so many identical shots? Well, unlike most subjects in front of a camera, astronomical targets are dim…very dim. Many are so dim they are invisible in the camera’s viewfinder. To collect the light from these objects (galaxies, nebulae, star clusters…etc.) you must expose the camera sensor for several minutes per photo, instead of fractions of a second as you would for daytime photography. Unfortunately, when you do this, the resulting image does not look very spectacular – it’s badly contaminated with noise.

Two images taken as 3-minute single exposures, noise is prevalent in both. Details such as the edges of the nebulae and faint stars cannot be seen. D Elijah.

Two images taken as 3-minute single exposures, noise is prevalent in both. Details such as the edges of the nebulae and faint stars cannot be seen. D Elijah.

These are 3-minute exposures of the Crescent and Dumbbell nebula in the constellations Cygnus and Vulpecula respectively. You can see the nebulae but there is also plenty of noise obscuring faint detail. This noise comes from different sources. The most prevalent being the random way photons strike the camera’s sensor – rather like catching rain drops in a cupped hand, you cannot be sure exactly how many photons or rain drops will be caught at any one time. A second source of noise comes from the fact that a camera does not perfectly read values from its sensor; some pixels will be brighter or dimmer as a result. Finally, a sensor’s pixels measure light within a limited range of values. If the actual value of light intensity for a given pixel is between two of these values then there will be an error in the reading. There are further types of noise in astronomical images such as skyglow, light pollution and thermal noise but these can be dealt with by calibrating the images – a rather complex process I will discuss in a future post!

By stacking multiple images, noise is reduced and the signal, like faint stars and subtle regions of nebulae, become more apparent. Photo sourced from www.dslr-astrophotography.com.

By stacking multiple images, noise is reduced and the signal, like faint stars and subtle regions of nebulae, become more apparent. Photo sourced from www.dslr-astrophotography.com.

The best way of dealing with this noise is to take many repeated exposures and combine (stack) them. This method takes advantage of the fact that each photo will differ because of the random noise they contain but critically they will all contain some amount of signal (the detail of the target you photographed). As you combine them, the signal (which is conserved across the pictures) builds in strength, while the noise tends to cancel itself out. The result is an image with more signal and relatively less noise giving more detail than you could ever see in a single photograph. To the left is a good example of the improvement in quality you might expect to see as you stack more photos or frames.

In addition, the bit depth of the image, which is the precision that an image can define a colour, also increases as you stack. For example, it you have a single 3-bit pixel (it can show 2³=8 values, i.e. from 0 to 7) a single image may measure the brightness of a star as 5, but the true value is actually 5.42. In this scenario, taking 10 photos, each giving the star a slightly different brightness value, may give you 5, 5, 6, 5, 7, 6, 4, 5, 5 and 6, the average of these being 5.4 – a more accurate value than the original, single shot, reading. The end result is a photo with lots of subtle detail that fades smoothly into the blackness of space.

So here are my final images of the Crescent and Dumbbell nebulae after I stacked over 40 frames each taking 3 minutes to capture (giving a total exposure of 2 hours each).

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Was it worth being bitten to death by midges, setting my dog off barking at 4am, putting my wife in a bad mood for the whole next day…I think yes!

Post by: Daniel Elijah

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The Human Sensor: Making the Invisible Visible

Breathe. Breathe deeply. Breathe in, breathe out. With each breath in, breathe in peace, tranquillity and calm. With each breath out, release tension, anxiety and pain. Let your mind be still, and your body relax, with an ever-present focus on your breath.

Such words and ideas may sound very familiar, and take you to a place of calm. Or they might sound completely foreign and a flight of fancy. The truth is, precious few of us in our daily lives ever consider our breathing outside of an escapist yoga class. But how many fewer of us, when we think about our breathing, take a moment to consider what might be in the air that we are breathing, and how that might be affecting us?

Air pollution is without doubt one of the biggest problems faced by the world’s cities. As estimated by the World Health Organisation, air pollution exposure causes 7 million premature deaths each year – one in eight of all global deaths. Whilst a significant number of these deaths occur in China (where there are estimated 4,000 premature deaths each day caused by air pollution) and India (where the non-smoking populace has a 30% lower lung capacity), Europe isn’t nearly as clean as it could be. A report from the EU’s European Environment Agency (EEA) says pollution is now the single largest environmental health risk in Europe, responsible for more than 430,000 premature deaths.

Closer to home, the picture remains grim. Manchester is the second most polluted city in the UK, and one of the most polluted cities in Europe. In Greater Manchester, the annual mortality estimate is over 1,000. But what actually are the pollutants that are causing all this damage?

One of the most significant is PM 2.5 , which is particulate matter condensed in air with a diameter smaller than 2.5μm (mainly sulphates, nitrates and carbon). These are nasty mixtures of combustion particles, metals and sulphates, and at less than 5% the diameter of a human hair, they can penetrate deep into the lungs. They have been linked to heart disease and lung cancer, and cause an estimated 29,000 premature deaths in the UK.

In addition, nitrogen compounds such as Nitrogen Dioxide (NO 2 ) form from the combustion process in vehicles. Long term exposure to NO 2 reduces lung capacity and lowers resistance to respiratory infection. The UK fails to meet the EU air quality standards for this pollutant, and exposure to NO 2 results in an estimated 23,500 premature deaths across the country.

According to the World Health Organisation, air pollution is the biggest public health problem faced by the developed world. But as we walk through busy streets, we never consider these effects. Apart from the odd stench of fumes from a bus or a lorry that we might notice, the fine particulates are undetectable to our senses and invisible to us. The cold statistics and hard science don’t relate to our daily experience. If we perhaps were more actively aware of how serious a problem this is, we might feel more inclined to drive less, or take more walks in the park, or simply avoid the busy streets. So how can we be more acutely aware of the science in our daily lives?

One way of connecting ourselves to certain issues and facts is through art. Music, dance and painting have all deeply emotionally resonated with us for millennia, in ways which science cannot. So scientific, socially conscious art could pave the way forward.

Screen Shot 2016-07-22 at 23.02.54In collaboration with Manchester European City of Science, the non-profit organisation Invisible Dust have commissioned the artist Kasia Molga to create a show in the streets of Manchester that brings this issue out into the open. Called the ‘Human Sensor’, dancers will wear futuristic suits that light up in different colours depending on what they are breathing, making tangible the effects of poor air quality.

These live performances take place across the 23rd-29th July, with the launch at 7:30pm on no.70 Oxford Road (formerly the Cornerhouse). Invisible Dust are also hosting an information space there, open from 23–29 July, 1–5pm weekends and 1–9pm weekdays with free drop-in talks and workshops every day.

If you want to bring yourself into the present, become more aware of your surroundings and the world around you, then focus on your breathing. But remember there is more to the world around us than what we see.

Guest post by: Carl Thomas

Learn more about the project here:

invisible dust

Human Sensor

 

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Are we ready to live without immunisations?

Screen Shot 2016-07-17 at 17.47.46The immune system is like an army, poised and ready to attack: it actually comprises two separate systems, these being the innate and the adaptive immune systems – you could think of these as two separate groups of soldiers i.e. foot soldiers and intelligence officers. The innate immune system responds quickly to threats, it is always on guard but this system is non-specific, meaning that it does not recognise any specific threats and will respond to all threats in the same way – this system could be thought of as the bodies foot soldiers (recognising all types of enemy but always launching the same type of attack). The adaptive immune system is slower since it needs time to recognise the threat but, once this is done, this system can launch a more specific, targeted, attack. This system also has a memory, meaning that after successive encounters with the same threat it will adapt and the next time it encounters the same threat its attack will be faster and more efficient. It is during this type of attack that antibodies are produced. These antibodies stick around in the body and help bolster our immune system and speed up future attacks (it is this process which is augmented through immunisation/vaccination). We could think of this system as the body’s intelligence agency, gathering information on its enemy and launching a targeted attack.

When we receive a vaccine we are attempting to induce an immune response without harming the body. The body is infected by a harmless version of a virus or bacteria that triggers an immune response without making the recipient sick. This then creates an immunological memory so that the next time we are infected by the same pathogen the immune system will be quick to react and the threat will be neutralised before we show any symptoms.

Vaccines have been a major success, they have helped to eliminate most of the childhood diseases that historically caused millions of deaths and are very cost effective. Thanks to this, average life expectancy has increased from 35 years in 1750 to above 80 years today. According to World Health Organization measles vaccination resulted in a 79% drop in measles deaths between 2000 and 2014 worldwide, and according to UNICEF each year immunisation prevents around 2-3 million deaths a year from life-threatening diseases in children.

But some people still choose not immunise their children, stating a range of reasons – from religion to the belief that vaccines are neither effective nor safe. In 1998 the Lancet published a paper by Andrew Wakefield stating that the measles vaccine produced autism in 21 children. Later several peer-reviewed studies failed to show any association between the vaccine and autism and eventually the Lancet’s editors fully retracted Wakefield’s paper claiming deliberate falsification. But, despite a lack of solid evidence and the paper retraction, vaccination rates in the UK dropped to 80% in the years following, leading to an increase in cases of measles across the UK – causing not only deaths but also measles encephalitis. By 2008, measles had become endemic in the UK due to low-vaccinated communities.

Last year there was a case of diphtheria in Spain when a 6-year-old non-immunised boy became infected. Diphtheria is a highly contagious disease caused by a bacterium called Corynebacterium diphtheria. Thanks to immunisation campaigns in Spain the number of cases of diphtheria in the country dropped from 1,000 cases in 100,000 inhabitants in 1945 to 0.10 cases in 100,000 in 1965 – now in 2016 diphtheria is thought to have been eradicated in this area. Therefore when this young boy fell ill last year there were no treatments available in the country at the time. Sadly, despite heroic efforts to import a treatment, the child died. When his parents were asked why he had not been immunised they said they felt tricked and not properly informed by anti-vaccination groups; they thought they were doing the best thing for their child.

So what happens when people decide not to immunise their children? :

Assuming that a large proportion of a population are immunised it is possible that non-immunised individuals may be protected by a process known as herd immunity. Basically, the more people who are immunised, the fewer opportunities a disease has to spread – this confers protection to those who can’t be immunised (such as children with cancer receiving chemotherapy or radiotherapy, children treated with immunosuppressed drugs such as corticosteroids, people with weakened immune system or people allergic to any of the components of the vaccine). This means that these people really depend on those around them being immunised.

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We can lose sight of the benefits of immunisation because we don’t have a memory of living in a world without vaccines. But, diseases that we thought were eradicated a long time ago will come back if we stop immunisation – meaning we could find ourselves confronting epidemics of diseases with the ability to kill hundreds of thousands of children and adults every year. Sadly some diseases will never be fully eradicated because they are found everywhere. For example, tetanus is a serious infection caused by Clostridium tetani bacteria which produces a toxin that affects the brain and nervous system. Clostridium tetani spores can be found most commonly in soil, dust and manure, but also exist virtually anywhere. So a child playing in a sand pit or with just some grass can get in easily infected through a cut or wound on his hands. Therefore, maintaining immunisation is particularly important in the fight against this type of disease.

Although vaccines do come with some side effects, like high temperature or soreness in the injected site, very serious health events post-immunization are rare and the benefits of immunisation clearly exceed the risks of an infection. Thus, the only way to prevent the infection is through immunisation.

Post by: Cristina Ferreras

References:

Rappuoli R et al. Vaccines for the twenty-first century society. Nat Rev Immunol. 2011 Nov 4;11(12):865-72. doi: 10.1038/nri3085. Erratum in: Nat Rev Immunol. 2012 Mar;12(3):225

UNICEF_immunization Facts and Figures April 2013 http://www.unicef.org/immunization/file/UNICEF_Key_facts_and_figures_on_Immunization_April_2013%281%29.pdf

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