What the frack?: An exploration of hydraulic fracturing in the UK.

For many years I’ve been skirting the sidelines of the debate on hydraulic fracturing (commonly known as fracking), occasionally dipping in and out of articles but usually concluding that I don’t know enough to make an informed decision. However fracking has now come to me, placing itself firmly on my doorstep – so I’ve decided it’s about time I did my research!

I live in Bury, a region in the north of Manchester which, according to the amusingly named website ‘Frack Off’, sits within what is known as an oil exploration block. This being an area of land, typically 1000s of square kilometres in size, which has been ‘awarded’ to an oil drilling and exploration company by the government. Apparently the lucky exploration company with control over my home turf is Hutton Energy.

screen-shot-2016-10-30-at-12-17-37

The reason my home county is such hot property for energy companies is because the ‘British Geological Survey Gas-In-Place Resources Assessment of Bowland Shale’ has suggested that it sits above a large amount of, possibly gas rich, shale rock. Shale is a fine-grained sedimentary rock formed by compression of mud (mineral particles and organic matter) over time. It is also incredibly common, forming over 35% of the world’s surface rock. Over millions of years shale becomes buried deep within the Earth and, when it reaches depths of over 2 kilometres, heat and pressure cause organic matter within the shale to release methane gas – it is this ‘natural gas’ which can be harvested to generate electricity for domestic use. The problem with shale gas is that, unlike conventional gas supplies (such as those harvested in the North Sea) which collect in large reservoirs, the methane in shale is trapped by the fine grain structure of the rock. It is only when shale rock is drilled and fractured that the gas is released and can be harvested. This process of fracturing shale rock to harvest methane gas has caused an enormous stir, with supporters on both sides of the debate campaigning ferociously.

But what are the debates for and against this process and how relevant are these to fracking in the UK?

To understand these arguments it is first important to know what hydraulic fracturing really entails and there is no doubt that the process sounds particularly invasive. For starters, shale gas exploration companies will drill large boreholes down into gas-bearing shale rock. These holes will stretch thousands of miles below the surface of the ground and, in many cases, will continue horizontally through the shale rock. These boreholes are then lined with steel and concrete for stability and to limit leakage of fracking-related materials into the surrounding land. Next, a perforating gun is used in the lower segments of the borehole to make a number of small holes in the concrete casing – these holes are concentrated in the parts of the pipe sitting within the shale rock. Finally, a mixture of water, sand and chemicals is pumped under high pressure down the borehole and out of the small holes in the concrete piping. This high pressure water mix causes fractures to develop in the shale rock, while sand within the water lodges in these cracks ensuring that they remain open and porous. This process allows gas trapped within the shale to flow out of the rock and then travel back up through the borehole to the surface for harvesting.

screen-shot-2016-10-30-at-17-15-27
Image credit BBC: http://www.bbc.co.uk/news/uk-14432401

Supporters of this process argue that fracking in the US has significantly boosted domestic oil production, driven down the cost of gas and created many job opportunities. Those in favour also suggest that fracking can generate electricity at half the CO2 emissions of coal – but, be aware that this figure varies depending on sources and that some argue that the atmospheric pollution caused by fracking is actually no better than that of traditional coal extraction. The benefits here are attractive for the UK, especially since our North Sea gas fields are reaching the end of their lives, most of our nuclear plants are planned to close by 2023 and a third of our coal-fired power stations are set to close by 2016 to meet European air quality regulations. So, we are undoubtedly in need of an energy boost. However, it is interesting to note that oil and gas industrial representatives recently told ‘New Scientist’ that “ it would take at least 10 years for the UK to produce a meaningful amount of shale gas, making it a poor substitute for dwindling North Sea production in the short term”

So is fracking fit for purpose, especially considering that many academics agree that a move towards renewable sources of energy is preferable?

Those opposed to the process argue strongly that fracking introduces too many health and environmental concerns to be a viable and safe source of energy. Specifically, many are concerned that methane gas and fracking chemicals could travel upwards through natural fractures in the rock, polluting underground aquifers and further contributing to global warming. It is also suggested that leaks in pipelines could lead to further aquifer pollution. These concerns are certainly valid, however to date there have been very few peer reviewed articles published suggesting that chemicals and methane released by the fracking process have reached local aquifers. It is also argued that these risks can be significantly minimised by strict regulations and regular monitoring. For example, thorough geological surveys should be carried out prior to exploratory fracking to detect pre-existing fractures, pipelines should be strongly reinforced and regularly monitored and chemicals used in the fracking process should be assessed and approved by the environmental agency.

Many opponents to the process also raise concerns that fracking may trigger earthquakes. Again, to date there have been few proven links between fracking and earthquakes. However, one of the few instances where this has been the case was in 2011 when two small earthquakes struck Blackpool close to an exploratory fracking site. Experts suggest that these quakes were caused by lubricated rocks slipping along a small fault line. Cuadrilla, the company in charge of the Blackpool site, propose that they will now monitor seismic activity around all their fracking sites and, if small quakes begin to occur, they will reduce the flow of water into the borehole, or even pump it back out preventing bigger quakes.

Indeed, many of the environmental and health concerns raised against fracking seem to be manageable given stringent regulation and proper monitoring – something which the UK government claim to take very seriously.

In my view more research is still needed to explore the validity of existing environmental concerns while stringent regulations must also be put in place before going forward with further exploratory work. This all leads me to one big question: can we trust those involved in the process to ensure this happens?

On a personal level I’m still not convinced, there does seem to be a strong vested government interest in moving fracking forward – in some cases this is happening to the detriment of local councils and areas of natural beauty. In my mind urgency is the mother of mismanagement so, until I’m convinced that fracking in the UK will be properly managed, local communities will be consulted and engaged as part of the process and this will not be used as an excuse to slow down on development of more sustainable energy resources I think I will remain skeptical.

Post by: Sarah fox

Save

Save

Light pollution – are we losing the night sky or is there still hope?

I guess it was inevitable that I would eventually write a post about light pollution – the modern day scourge which reduces the visibility of celestial objects and forces astronomers to travel hundreds or sometimes thousands of miles in order to avoid it. There’s even a saying that an astronomers most useful piece of equipment is a car! Probably the most damaging effect of light pollution is not that it makes faint galaxies and nebulae difficult to spot and photograph (there are ways of overcoming this), but that whole generations of children grow up not knowing what a truly dark sky looks like!

Figure 1. The effect of light pollution on the night sky. This split image shows how artificial light washes out most of the faint detail in the constellation Orion.
Figure 1. The effect of light pollution on the night sky. This split image shows how artificial light washes out most of the faint detail in the constellation Orion.

 

I am one of those children. I grew up in suburban England (about 60 miles north west of London) where the night sky had a beige/orange tinge, the constellations were difficult to spot and the Milky Way was something you either looked up in a book or ate. I was about 14 when first I saw a proper night sky; on holiday in North West Scotland. I was so fascinated with the sight that an interest in astronomy embedded itself in me and never left! I was lucky, I was still quite young and my interest could be nurtured before the realities of life (exams, chores, jobs…) stepped in. Many aren’t so lucky. I always wonder, how many inquisitive people never experience the joy of observing the universe because of that orange glowing veil of light pollution (LP). It is the barrier that light pollution creates that prompted me to write this post.

I will now concentrate on the issues LP poses to astronomy. Before I do so, I should say that good evidence exists showing that LP can negatively affect human health (such as disrupting sleep cycles) and the natural environment (changing bird migration patterns etc), detailed discussions can be found here. Regarding astronomy, light pollution is

Figure 2. Direct light pollution. These street lights in Atlanta radiate light across a wide area, stargazing near these will be very difficult. Image taken from http://www.darkskiesawareness.org
Figure 2. Direct light pollution. These street lights in Atlanta radiate light across a wide area, stargazing near these will be very difficult. Image taken from http://www.darkskiesawareness.org

problematic for two main reasons. (1) Unwanted light can travel directly into your eyes ruining the dark adaption they need to observe faint celestial objects. It can also invade telescopes causing washed out images and unwanted glare. This form of light pollution involves light traveling directly from an unwanted light source (such as a street lamp) to your eye/telescope.

The second source of LP comes from the combined effect of thousands of artificial lights, known as sky glow. Sky glow is form of LP most people are familiar with; the orange tinge that

Figure 3. Skyglow in Manchester. This light is scattering off the atmosphere and falling back to the ground. As a result, the sky looks bright orange. Image taken from https://commons.wikimedia.org/
Figure 3. Skyglow in Manchester. This light is scattering off the atmosphere and falling back to the ground. As a result, the sky looks bright orange. Image taken from https://commons.wikimedia.org/

in some places can be bright enough to read by! Sky glow exists because the Earth’s atmosphere is not completely transparent, it contains dust, water droplets and other contaminants that scatter man made light moving through it. Some of this light is scattered back down towards the Earth, it is this scattered light that drowns out the distant stars and galaxies. It is a visual reflection of the amount of wasted light energy we throw up into the sky.

You may be thinking that LP spells the end for astronomy in urban areas. Well luckily there are ways around the problem. One way is to  filter it out. The good thing about skyglow is that it is produced mainly by street lamps that use low pressure sodium bulbs. The light from these bulbs  is almost exclusively  orange with 589nm wavelength. Figure 4 shows a spectrum of the light given out by one of the lamps.

Figure 4 - Different colours of light produced by a typical low pressure Sodium street light. The vast majority of the light is orange (589nm) as shown by the bright orange bar. Image taken from: https://commons.wikimedia.org/
Figure 4 – Different colours of light produced by a typical low pressure Sodium street light. The vast majority of the light is orange (589nm) as shown by the bright orange bar. Image taken from: https://commons.wikimedia.org/

Since this light is comprised of essentially one colour, we can use a simple filter to cut out this wavelength whilst leaving other wavelengths unaffected. In addition, the wavelength of the sodium lights is quite different from the colours produced by many nebulae. Therefore when we filter out the orange light, we don’t also block the light coming from astronomical objects.

So…what am I worrying about then? If light pollution can be overcome by filtering out certain wavelengths of light then astronomy should be possible from anywhere. Well, not quite. Filters are not perfect, even the best filters will block other colours and dim our view of the stars. There is also another reason to worry – street lights are changing. As you may

Figure 5 - LED and sodium streetlights outside my house. LEDs produce light that is harder to block using conventional filters, Sodium lights (seen here as orange) shine lots of light into the sky contributing to sky glow. (Image is my own)
Figure 5 – LED and sodium streetlights outside my house. LEDs produce light that is harder to block using conventional filters, Sodium lights (seen here as orange) shine lots of light into the sky contributing to sky glow. (Image is my own)

already know, street lights are being altered from the sodium bulbs to LEDs. These LEDs are more energy efficient and produce a more natural white light. However, this white light is harder for astronomers to filter out without also blocking light coming from deep space. Luckily, these newer lights are better at directing their glow downwards towards the ground rather than allowing it to leak up into the sky. Figure 5 shows the LED and Sodium lights outside my house. The LED lights appear darker because most of their light is directed towards the ground.

There is still debate in the astronomy community about whether the new street lighting will be beneficial for astronomy. At the moment, LEDs are being introduced slowly so it is difficult to make a clear comparison. My hunch is that when Sodium lights are replaced completely, there will be an improvement in our night skies and finally young people will grow up seeing more of the night sky.

Post by: Daniel Elijah

 

Save

Could fruit flies help defeat HPV-derived cancers?

In 2012 528,000 cases of cervical cancer were diagnosed worldwide. In the same year, more than half this number were estimated to have died as a result of this condition. The cause? A virus of the Papillomaviridae family, specifically one of the High Risk Human Papillomaviruses (HR-HPVs). Although mainly associated with cervical cancer in women, HR-HPVs cause an ever increasing number of head and neck, throat and genital tumours in both sexes.

Human Papillomaviruses lack an envelope, a coat made from the membrane of the host cell, possessing only an icosahedral capsid – a sturdy protein bubble that protects the viral DNA within. Viral DNA hijacks the host’s cellular machinery to produce new viral proteins which both continue virus assembly and cause cancer. It is still uncertain exactly how these proteins interact with our cells to cause cancer but some major players and pathways have been identified. Specifically, scientists believe that two particular proteins (the E6 and E7 proteins) may play an important role in this process.

These two E6/7 macromolecules can be referred as “oncoproteins”. Although quite scary, this term simply defines proteins which are involved in mechanisms that could cause a cell to behave abnormally, increasing the chances of them becoming cancerous. Specifically, these two proteins interfere with a wide variety of mechanisms that will trigger conversion to malignancy. Respectively, they either boost or block the activity of p53, Rb and E2F, three molecules that control a cell’s life cycle.

Considering the huge impact such cancers have on human life, it may seem unusual that we are still in the dark about so many aspects of HPV associated pathophysiology. Our limited knowledge is in part due to constraints implicit in this type of research. Specifically, for obvious ethical reasons, researchers are not able to study HPV associated cancers in living human subjects or deliberately induce cancers in subjects. Therefore, they must rely on model systems when studying these disorders. In the past, researches have used artificial keratinocytes (skin’s cells) and mouse models, to understand how processes work in living tissues. However, this work raises a few questions, such as: How do you compare findings in tissue alone to what you would find in a dynamic and complex living system and how well can we compare mouse models to human conditions?

screen-shot-2016-10-10-at-19-43-34
Picture credits: By Botaurus, via Wikimedia Commons – CC BY-SA 2.5 (open access/open use).

We now have an answer to these questions, or at least something that marks the start of a deeper understanding. Researchers at the University of Missouri have been able to successfully develop and use living, fruit fly models. Mojgan Padash’s research team injected fruit flies with the E6 protein along with a human-derived one needed by the E6 to function. The first results show that, although abnormalities in the fruit flies’ skin were noticed, another molecule was needed in order to fully trigger cancer. Following the hypothesis that mutations in a human molecule called Ras, a family of “switch” proteins which activate cell growth-specific genes, the team introduced the latter into the fruit flies. Those “simple” abnormalities turned into malignant cancers, just as they would do in humans.

The results, published in the open access journal PLoS Pathogens, allow scientists to monitor biochemical pathways similar, if not identical, to those found in human sufferers. But why flies and not mice? Although further away from humans, sharing only 60% of the human genome against the 97.5% of mice, flies are easier to use than their murine counterpart. Fruit flies are easier to breed (so to quickly obtain new generations) and their genes can be mutated quicker than mice. Moreover, little to no ethical approval is needed to use them (they can be ordered online, with just one click!) and their easier to monitor development allows researcher to effectively model disease development. These fruit fly models, which are continuously refined and developed, have the potential to help in discovering new molecules involved in such processes.

It comes to no surprise that such information could impact heavily on future treatment, and even the prevention of pathologies caused by this increasingly dangerous family of viruses. So, next time you think about killing a fruit fly in your kitchen … maybe think twice.

Post by: Paolo Arru – @viraleclair

screen-shot-2016-10-10-at-19-43-41Paolo is currently a final year student in Microbiology at the University of Manchester, UK. Science communicator wannabe, he has a keen interest on everything related to HPV, viral oncology and parasitic infections to just say a few. Every bit of his free time is used for planning and getting involved in new projects, baking and getting lost in museums. You can follow him talking about science festivals, geeky stuff and bake off on

Save

Save

Symbiosis – harmony or harm?

We have all experienced relationships which are beneficial and others that are not. The same can be seen throughout nature. Originally defined by German scientist Heinrich Anton de Bary, symbiosis describes a close association between two species, principally a host and a symbiont, which lives in or on the host. While some partnerships may be advantageous or neutral to one or both parties, others may have a more detrimental effect.

Mutualistic symbiosis:

screen-shot-2016-10-02-at-22-27-45The first of the symbioses involves relationships between two different species which benefit both organisms. Mutualistic symbiosis can involve organisms of all shapes and sizes from stinging ants and bullhorn acacia trees, a relationship where the tree provides the ants with food and shelter in return for protection from herbivores, to the alliance between oxpeckers and zebras, in which the bird enjoys a readily available food source while the zebra has any parasites living on it removed.

One of the most well studied forms of mutualistic symbioses is that of the ruminant (i.e. cattle and sheep etc.), as these organisms play an important role in our agriculture and nutrition. Ruminants host an extensive microbial population in the largest of their four stomachs, the rumen. A mutually beneficial relationship exists between these two organisms because the rumen microbes are able to digest the plant matter consumed by the ruminant. In doing so, they produce fatty acids, which can be used by both parties for energy. Carbon dioxide is also released in this process, providing the rumen microbes with the oxygen-free environment they need to survive (these microbes are predominantly anaerobic so are poisoned by oxygen).

Parasitic symbiosis:

screen-shot-2016-10-02-at-22-27-52In contrast to mutualistic symbiosis, the interaction between two organisms may be less savoury in nature. Parasitic symbiosis describes a relationship between organisms where the symbiont benefits at the expense of its host. Unfortunately for the host, this generally causes it harm, whether this be in the form of disease, reduced reproductive success or even death. The symbiosis between birds, such as the cuckoo and the reed warbler, known as brood parasitism, is a characteristic example of a parasite-host relationship. Rather than building her own nest, the parasitic cuckoo will lay her eggs in a reed warbler’s nest, leaving the warbler to raise this egg along with her own offspring. Once hatched, the cuckoo chick then ejects the warbler’s young from the nest, allowing it to receive all the food that its “adopted” mother provides.

Unsurprisingly, this antagonistic relationship has led scientists to question why warblers raise these parasitic chicks if the practice is so harmful. It has been suggested that cuckoos engage in a kind of “evolutionary arms race” with its chosen host, based on the host’s ability to recognise a parasitic egg. In this ongoing contest, the evolution of a host species to become more adept at spotting and rejecting a parasitic egg may result in a subsequent evolution in the cuckoo to counter this change. This may be to lay eggs with greater similarity to the host’s or to move towards a new host species. Such a process could continue indefinitely.

screen-shot-2016-10-02-at-22-28-01An even more detrimental relationship exists between the parasitoid wasp and its hosts, which include a range of insects from ants to bees. Similarly to cuckoos, these wasps rely on their host to facilitate the development of their young, but do so by either laying their eggs inside the host or gluing them to its body. Once hatched, the wasp larva will feed on the host, usually until it dies.

Commensal symbiosis:

Symbiosis does not necessarily have to be beneficial or detrimental to the host organism. Commensal symbiosis describes a relationship in which one organism benefits while the host is unaffected. This may be in the form of shelter, transportation or nutrition. For example, throughout their lifecycles small liparid fish will “hitch a ride” on stone crabs, providing them with transportation and protection from predators while conserving energy. The crabs, meanwhile, appear to be neither benefitted nor harmed.

One case of commensalism which may come as a surprise involves Candida Albicans, a species of yeast known to cause the fungal infection Candidiasis in humans. Contrary to popular belief, C. Albicans can be pathogenic or commensal depending on which phenotype it has. Under normal circumstances, C. Albicans reside in our gastrointestinal tract undergoing a commensal symbiotic relationship with us (i.e. causing us no harm). This interaction is actually the default existence for C. Albicans. When changes occur in the body’s environment, however, a “switch” in phenotypes to the pathogenic form can occur, placing a temporary hiatus on the usual commensal relationship.

A plethora of symbiotic relationships exist throughout the natural world, from the tiny microbes inhabiting the ruminant gut to the large acacia trees housing ants. They can offer both organisms the harmony of a mutually beneficial association, as is the case with the oxpecker and the zebra, or be parasitic and work in the favour of one player while harming the other, as seen with the parasitoid wasp. In some instances, one organism can gain benefit without impacting the other either positively or negatively. As illustrated by C. Albicans and cuckoos, a symbiotic interaction may change or evolve according to the environment or evolution of the host, respectively. Symbiosis is clearly a highly important aspect of nature which many organisms rely on for survival, and one that will continue to fascinate scientists and non-scientists alike both now and in the future.

Post by Megan Barrett.

Cakealicious science: The science of baking

screen-shot-2016-09-26-at-08-16-07Food glorious food! Cakes cakes and more cakes! These sweet creations have had people drooling for centuries. There are many variations from rich chocolate to fruit and nut, covered in buttercream or marzipan, stuffed with jam or cream, the choices are almost endless. They’re perfect for big celebrations or just a chilled out half hour with a cup of coffee. But how on earth do they actually work? How can butter, sugar, flour, eggs and baking powder combine to make a delicate mouth-watering sponge?

Magic?

screen-shot-2016-09-26-at-08-15-46Well science magic anyway. Each key ingredient has its own special role, without which the cake would collapse. The major ingredients need to be roughly of equal weights. First off the sugar and fat are mixed together. During the mixing process air gets caught on the rough surface of the sugar granules and is sealed in by a film of buttery fat, this forms a light fluffy mixture akin to whipped cream. We use caster sugar in this process rather than granulated sugar because it is finer than granulated sugar and therefore has a greater surface area on which to trap air.

screen-shot-2016-09-26-at-08-16-25But sugar does more than just trap air within the cake batter. It softens the flour proteins tenderising the mixture, it also lowers the mix’s caramelisation point, allowing the crust to develop a crisp golden consistency at relatively low temperatures. Finally, sugar also helps keep the cake moist and edible for many days. Most of the moisture in a cake comes from the eggs, which provide the mix with the majority of its liquid. When everything is mixed together the eggs produce a foam which surrounds the air bubbles in the mixture protecting them from the heating process and which is also stiffened by starch in the flour. Proteins in the flour join together creating a network of coiled proteins that we know as gluten. Gluten is key to holding the cake together, it expands during baking and then, when cooling, coagulates and is able to support the cake’s weight.

For the bakers out there you may have noticed that we have missed out the baking powder, this may come across as some voodoo magic but it is basically just dried acid and an alkali. Adding water and heat to this mix allows them to react producing CO2.

Now it’s not just getting the right measurement of ingredients, but it’s also essential to get the temperature of the oven precisely right. Too low and the expanding gas cells coagulate producing a coarse heavy texture leading to the cake sinking, too hot and the outside starts setting before the inside even finishes baking, leading to a volcano-looking cake.

So when you next grab a cupcake just take a little time to appreciate the exact science that went into baking that mouth-watering little treat. So many things that could go wrong it’s a miracle we ever found out how to make these soft icing covered delights.

screen-shot-2016-09-26-at-08-22-22

Post by: Jennifer Rasal

Sources:

https://www.theguardian.com/science/blog/2010/jun/09/science-cake-baking-andy-connelly

https://en.wikipedia.org/wiki/Cake

Save

Save

Woody Plants and pharmaceutics

Take a moment to think about your health over the last year. How often have you taken a painkiller to manage that headache or fever? These powerful tools have the ability to save you from a day of pain, allowing the survival of that long shift at work or half-marathon which has slowly crept up on you. How many relatives or friends have had their health improved through life saving medications such as chemotherapy or anti-depressants. There are a large variety of medications widely used today that have transformed our lives and we would struggle in a world without them. Many are aware that it is advances in medical research which have enabled the development and availability of these. However, it is often forgotten that when developing such drugs scientists will usually take their inspiration from similar compounds found in nature. But where? This article gives much deserved recognition to nature’s own pharmacologists. After all, these magicians are our true heroes.

So, what natural marvels are responsible for these compounds? – mainly plants, animals and fungi. This article will focus primarily on woody plants and their ability to produce useful chemicals. The extraction of compounds from plants goes back years. From tribes making herbal remedies to the scientific extraction of the chemicals we use today. Below are a few examples of how woody plants have completely transformed our lives:

Aspirin:

screen-shot-2016-09-19-at-20-04-45Aspirin is a silicate sold as an over the counter medication. Its main purpose is to reduce pain and inflammation. The active ingredient in this common drug originally comes from willow tree bark and has actually been used for about 6000 years. So, how does this drug work? Willow bark contains a substance called salicin which the body transforms into salicylic acid. This acid reduces the production of certain prostaglandins in our nerves. Prostaglandins are produced in response to tissue damage or infection, their role being to facilitate the healing process. However, alongside their healing properties they also cause pain, therefore reducing their production can minimise the pain associated with the healing process. It can subsequently be deduced that willow trees do much more for us than just creating a gorgeous aesthetic landscape!

Irinotecan:

screen-shot-2016-09-19-at-20-05-23Irinotecan is a chemotherapy medication primarily used to treat colon and rectal cancer. The active ingredients within this medication include camptothecin, pentacyclic quinolines and 10-hydroxycamptothecin, which are derived from Camptotheca Trees, Camptotheca acuminata. The mechanisms by which these compounds interact with the human body are complex. They inhibit DNA topoisomerase I which is important for the replication of cancer cells. It would therefore make sense that without this substance, cancer cannot thrive. This is because type 1 topoisomerases are catalysts for the transient breakage of DNA and for the re-joining of the strands following this during cell replication. Without this catalyst, replication would occur at a very slow rate. Cancer is a devastating disease and advances such as this are hugely important.

Digoxin:

Top: Normal heart activity. Bottom: Heart fibrillation
Top: Normal heart activity. Bottom: Heart fibrillation

Digoxin is well established in the treatment of heart arrhythmias including atrial fibrillation. It is extracted from the leaves of the common foxglove plant, Digitalis purpura. It works by slowing down the heart alongside improving ventricle filling which increases the blood supply available for each pump. The heart is one of the most important organs in the body, subsequently reflecting the importance of this medication and its lifesaving qualities.

These are just three examples of how woody plants have transformed our lives. However, there are still many unidentified species that have not yet been discovered in our ecosystems which have the potential to contain life-saving chemicals. In addition, there is the potential for the availability of medication that has fewer side effects to those currently in use. Unfortunately, many biomes are currently being destroyed at such a rate new species, and perhaps medically active chemicals, are being removed before any possible benefits can be uncovered. Therefore, the increased rates of deforestation may be destroying more than just habitats, they may be taking with them a wealth of potentially undiscovered medicines. This is just one more example of why conservation work is so important and I urge that it is taken seriously. Effective conservation is clearly vital to improve the lives of our future generations. It can be concluded that plants have played a huge role in our lives over many generations and continue to help us on a daily basis thus reflecting the importance of conserving them.

Take home message: Next time you take that aspirin in a moment of despair, take a moment to really appreciate the unsung heroes of pharmacy – woody plants. It is a shame that whilst many plants save us, we thank them by cutting them down, destroying biomes and causing extinction.

Post by: Alice Brown


References:

http://medicinalplants101.blogspot.co.uk/2014/01/camptotheca-aka-cancer-tree.html

http://sitn.hms.harvard.edu/flash/2011/where-does-medicine-come-from/

http://www.arthritisresearchuk.org/arthritis-information/complementary-and-alternative-medicines/cam-report/complementary-medicines-for-rheumatoid-arthritis/willow-bark.aspx

http://www.biologicaldiversity.org/publications/papers/Medicinal_Plants_042008_lores.pdf

http://www.ebi.ac.uk/interpro/entry/IPR018521)

http://www.kew.org/science-conservation/plants-fungi/digitalis-purpurea-common-foxglove

http://www.sciencedirect.com/science/article/pii/S1319610310000578

https://www.bhf.org.uk/heart-matters-magazine/medical/drug-cabinet/digoxin

https://www.drugs.com/aspirin.html

https://www.google.co.uk/search?q=Irinotecan&biw=1366&bih=667&source=lnms&tbm=isch&sa=X&ved=0ahUKEwiygLePlu7NAhXJB8AKHRwJBloQ_AUIBigB#imgrc=kiktTvOYld7YIM%3A

https://www.google.co.uk/search?q=type+1+topoisomerase&biw=1366&bih=667&source=lnms&tbm=isch&sa=X&ved=0ahUKEwishr_Uke7NAhULAsAKHZxHAeIQ_AUICCgB#tbs=sur:fc&tbm=isch&q=arrhythmias+&imgrc=rri9FbPzjvwvoM%3A

https://www.google.co.uk/search?q=willow+tree&biw=1366&bih=667&source=lnms&tbm=isch&sa=X&ved=0ahUKEwjxs7bnje7NAhXoC8AKHQhNC2YQ_AUIBigB#q=willow+tree&tbm=isch&tbs=sur:fc&imgrc=nDpmo_llPSg_1M%3A

Save

Are we finished editing CRISPR?

The academic world has been abuzz in the last few years with talk of a new gene editing technology known as CRISPR.  We hear about it on the news and are told that it could one day be a game-changer for modern medicine in terms of genome editing. But, like this article, all new techniques require proofreading and adaptation. So what I’m really wondering is: are we finished editing CRISPR?

CRISPR stands for ‘clustered regularly interspace palindromic repeats’, a mouthful even in the scientific community! CRISPR is a constituent of prokaryotic DNA and is used by these cells as a simple immune system, protecting them against viral attacks. We can imagine prokaryotic DNA as a piece of string (below: labeled as bacterial DNA), with repeated segments (circles) broken up by spacers (rectangles). Bacteria are able to detect invading viral DNA and add short sequences from the viral DNA in between the repeated sequences of their own DNA, creating a catalogue of past infections (a bit like our own immune system). If a virus attacks the same cell again these spacer regions are recognised by a special group of proteins called Cas proteins.  Cas proteins are nucleases which use the CRISPR-incorporated viral DNA segments to chop up the infecting viral DNA and inactivate it.

screen-shot-2016-09-11-at-13-39-39

Scientists have harnessed the power of the CRISPR/Cas9 system by replacing viral DNA spacers with synthetic guide RNA’s that match a specific DNA sequence – this can be anything the scientist wants to modify. Researchers can then direct the Cas9 protein to their selected gene, causing a break in the DNA and the deletion of that region of the gene, ultimately allowing them to control expression of selected genes.

In theory CRISPR has the power to edit and even remove harmful genes associated with both acquired and hereditary diseases. In fact, just this year Anderson and colleagues at MIT demonstrated its potential in mice, correcting a harmful metabolic mutation. So why are we not using CRISPR in the clinics already?

While most people have no issue with treating acquired conditions, such as cancer, in previously healthy people, concerns arise when we talk about germline editing: i.e. editing human embryos prior to birth. From a medical perspective embryo editing could enable children with life threatening and debilitating conditions to lead a ‘normal life’. However, some parents believe that editing their child’s genome will change the child’s identity. Researchers also argue that, not only will germline editing reduce genetic diversity but we also don’t know enough about the genome and its regulation to confidently make such drastic and heritable changes. On a personal note, my main concern is where would germline editing stop? Where do we draw the line at disease state? For example obesity, my own area of research, and its predisposition is now considered as a disease.  The more conditions we begin label as ‘diseases’ the easier it could be to edit for desired traits.

All these issues exist before we even begin to think about the safety aspects of this new technique.  How do we deliver this system effectively into the human body? And, once there, how efficient and specific will it be. For example off target effects have ranged between 0.1-60%, levels still too risky for the clinics.

While acknowledging that CRISPR does have great potential in the future, much editing and rewriting may still be required before we can click submit.

Post by: Stephanie Macdonald

Sources:

http://www.nature.com/news/crispr-1.17547

http://www.nature.com/articles/nbt.2884.epdf?referrer_access_token=vn4y2fRlT6MSfnjiTkEah9RgN0jAjWel9jnR3ZoTv0NYT9zJj6mpbqWqBhkZTqLWByT9ZihiHupT0fSw150iFynOlHiUTmOgoLqeCBiezScmQzKXSWZlhANyZY8taAUjw7mxZP3DyqCYVeWMBSDBoB_ExZ0FQkLTfyBfhnOubzmO0jxfwklUENzc3pAW-hXzt-7A-uc2YpLGwekIaMKzouz-lsbrPIE9Dozc5RIYLf8%3D&tracking_referrer=www.nature.com

Figure adapted from:

https://en.wikipedia.org/wiki/CRISPR

Save

How to perfect your astro-photos.

In my last post I discussed why astronomers take multiple identical photographs of the same astronomical object in order to reduce the effects of random noise. I discussed how this noise arises and gave examples of the improvements gained by stacking multiple photos together. Of course, reducing random noise within your image is an important first step but, if you really want to obtain the perfect astro image, there is still more to consider. Both your camera and telescope can introduce a number of inconsistencies in your images, these occur to the same extent in every photograph you take, meaning they cannot be cancelled out like random noise can. Here I will discuss what these inconsistencies are and the ways astrophotographers remove them.

So…what are these inconsistencies? Well they come in three types and each must be dealt with separately:

The first of these is a thermal signal which is introduced by the camera. This tends to look like an orange or purple glow around the edge of an image. It develops when heat from the camera excites electrons within the sensor. As we take a photo, these heat-excited electrons behave as though they have been excited by light and produce false sensor readings. This effect gets stronger with increasing exposure time and temperature. The best way to remove this is to take an equal length exposure at the same temperature as your original astro image but with no light entering the telescope/camera (perhaps with the lens cap on). The resulting picture will contain only the erroneous thermal glow. This ‘dark’ frame can then be subtracted from the original image.

fig_1
Figure 1. The original exposure (showing the constellation Orion at the bottom) shows a strong thermal signal in the top left. By taking a dark frame of equal exposure, we can subtract out the thermal signal, giving a better result.

The next inconsistency is known as bias. This constitutes the camera sensor’s propensity to report positive values even when it has not been exposed to light. This means that the lowest pixel value in your picture will not be zero. To correct this, it’s necessary to shoot a frame using the shortest exposure and the lowest ISO (sensitivity) possible with your kit then subtract it from the original frame. For most modern DSLR cameras, this subtraction has a very small effect but it does increase the contrast for the faint details in the picture – which is particularly important when shooting in low light.

Finally, and arguably the most important image inconsistency of all – uneven field illumination. This problem occurs when the optics within a telescope do not evenly project an image across the camera’s sensor. Most telescopes (and camera lenses) suffer from this problem. A common cause of uneven illumination is dirt and dust on the lens or sensor, which can reduce the light transmitted to parts of the sensor.

This is the objective lens from my telescope before and after cleaning. Although small specs of dust do not seriously affect the overall quality of the image, they can contribute to uneven brightness in the image.
This is the objective lens from my telescope before and after cleaning. Although small specs of dust do not seriously affect the overall quality of the image, they can contribute to uneven brightness in the image.

The final cause of uneven illumination is vignetting, this is a dimming of the image around its edges. Vignetting is normally caused by the telescope’s internal components such as the focus tube and baffles (baffles stop non-focused light entering the camera). These parts of the telescope can restrict the fringes of the converging light from entering the camera. So how do we combat this…keep cleaning the lens? Rebuild the internal parts of the telescope?…no. The answer is simple; take a ‘flat’ calibration frame. All you need to do is take an image of a evenly illuminated object (such as a cloudy sky, white paper, or blank monitor screen). Since you know the original scene is uniformly bright, any unevenness in the brightness of this image must be due to issues with the telescope. You then divide the brightness of the pixels in the original image by the pixels in the flat frame and magically, the unevenness is gone.

For your enjoyment, here’s some examples of flat frames taken from across the Internet, the middle image is from my scope. There are some diabolical flats here; I wonder if it’s even possible to conduct useful astronomy with such severe obstructions in a telescope!

Some examples of flat field frames taken by different telescopes. All these frames show were light is being blocked from reaching the camera sensor. My telescope’s flat frame is the middle picture; it looks good in comparison.
Some examples of flat field frames taken by different telescopes. All these frames show were light is being blocked from reaching the camera sensor. My telescope’s flat frame is the middle picture; it looks good in comparison.
By applying the flat frame correction, the background of the image becomes more even, and dark patches due to dust disappear! No need to clean your scope! (Image taken from http://interstellarstargazer.com).
By applying the flat frame correction, the background of the image becomes more even, and dark patches due to dust disappear! No need to clean your scope! (Image taken from http://interstellarstargazer.com).

For many people starting to turn their cameras and scopes to the heavens, all of this does sound rather arduous but there is software out there that will automatically combine your star images with the three calibration images and spit out what you want (see Deep Sky Stacker). I was amazed that for reasonably little effort and no extra money, I could improve the quality of my images significantly.

Post by: Daniel Elijah

 

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]

Save

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!

Share This