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Thanks to everyone who came to the 2011 Christmas Lecture, it was a great evening. If you have any comments don’t forget to get in touch, we’d love to hear from you!
Christmas Lecture 2011
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Dragon’s Den – Brainwaves Style!
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So, it’s turning into an exciting year for Science Brainwaves, but we’re still on the lookout for the next innovative and exciting public engagement event! This is where we want you – our current/new/never before – volunteers! Do you think our current events’ listing is missing something? Have you got a fantastic idea? Need some money and help putting it together and marketing it? Then we have the PERFECT opportunity for you!
We are offering £250 to the best brand new event/workshop idea! In return all we ask is that you submit a summary of your idea (no more than 500 words) to: dragonsden@sciencebrainwaves.com by Tuesday 1st November. We will then select the best 10 and ask you to pitch your event idea to a panel of expert judges on Tuesday 22nd November, 8pm, Coffee Revolution.
We are open to any idea, be it a lecture, a debate, a new science experimentation workshop which could be hosted at schools and colleges, an adult event, an event for families, for children, for men/women, boys/girls – we really don’t mind! Our only request is that the event somehow can be linked to the British Science Association National Science and Engineering Week 2012 theme – ‘Our World in Motion’ – this is such a broad title, we really feel anything could be fitted into it somehow!!
In addition to the £250 prize money, we will support your event 100%, allowing you access to our large media and ‘useful’ contact network. Offering any advice needed, whether that’s how to promote the event, finding additional funding, where to find the best venue, recruiting volunteers or even what colour scheme would work best!
Please check out the ‘Science Brainwaves does Dragon’s Den’ Rules below for further information – but if you have any more questions please feel free to submit them to the email address detailed above.
Many thanks!
For a detailed list of the rules please click here.
Transparent tissues offer a window into the brain
By Kathryn Higgins
A revolutionary reagent has been developed that can literally turn biological tissues transparent. Researchers from the RIKEN Brain Science Institute in Japan have developed a reagent which allows 3D imaging of the neuronal network deep inside a mouse brain.
Imaging and labelling of cell populations deep within tissue has been a challenge for scientists for many years. Although advances have been made in cell imaging there are still many obstacles to overcome. Tissues often have to be sliced 1mm thick for viewing under a microscope to dissect networks since imaging within deep tissues leads to many problems due to the lack of transparency of the tissue. Several clearing solutions have been developed but these have disadvantages such as expense and quenching of fluorescently labelled proteins that are often used in cell research to visualise the structures.
A research team led by Atsushi Miyawaki, however, have recently developed a reagent, after a chance observation, which may revolutionise deep tissue imaging by obtaining 3D images that are valuable for improving our understanding of biological organisms and how they function.
The reagent, called ScaleA2, is a highly effective clearing reagent, greatly improving the transparency of tissues, and stabilising fluorescently labelled proteins. This allows imaging to be done at a much greater depth than currently possible, providing detailed 3D visualisation of neuronal networks within the brain than has ever been managed before.
Current research using ScaleA2 was done using dead embryo tissue for imaging neurones and blood vessels deep inside the mouse brain. Miyawaki and his research team, however, believe that the scope for using ScaleA2 in other tissues and organisms is not limited, and are currently trying to optimise the reagent for use in live tissue. This would open the door to experiments that have never before been possible.
Image shows two murine embryos. The left embryo was placed in PBS, whilst the embryo on the right was incubated for 2 weeks in ScaleA2 solution.
Reference:
Hama et al, (2011) Scale: a chemical approach for fluorescence imaging and reconstruction of transparent mouse brain. Nature Neuroscience. Ahead of print.
The paper can be found at:
http://www.nature.com/neuro/journal/vaop/ncurrent/pdf/nn.2928.pdf
A Sweet Way to Heal Wounds
By Kathryn Higgins
We’ve all heard the term rubbing salt into the wounds, but using sugar instead may be a new treatment for wound healing and reducing pain.
Moses Murandu, a Senior Lecturer in Adult Nursing at the School of Health and Well Being at the University of Wolverhampton, Birmingham, has just been awarded a £25,000 grant to continue a study in the effect of sugar on wounds and cuts.
Originally raised in Zimbabwe, Moses grew up following traditional African remedies, one of which involved treating wounds with cane sugar. Trained as a senior nurse, Moses was surprised to find that this was not common practise when he came to the UK stating “when I was a child, my father used sugar or salt and I grew up without realising that something that works is not widely used”.
Leading a study at Selly Oak Hospital in Birmingham, involving 21 patients whose wounds had not responded to conventional treatment, Moses poured granulated sugar onto bed sores, leg ulcers or amputations before the wound was dressed. However, he did point out that the sugar used was not taken straight off the supermarket shelves, but was certified, sterile sugar direct from the manufacturer.
The study found that a solution of 25% sugar was effective in not only reducing pain associated with wounds, but also improved healing. The sugar solution works by drawing water out of the wound into the dressing. Bacteria need water to survive so when sugar is added bacteria are killed leading to healing of the wound and reducing pain.
An abstract of this work was submitted by Mr Murandu to the Fondation Le Lous, and was awarded the Fondation Le Lous Research Innovation Award and £25,000 to continue his research for a further two years.
This innovative practise would save the NHS millions of pounds a year, with treatment costing about £1.49 each time compared to hundreds of pounds to hire equipment to drain wounds.
For further details of the study see:
http://www.wlv.ac.uk/default.aspx?page=24330
http://wlv.ac.uk/default.aspx?page=21067
Science and cartoons
Guest post from Caroline Parkin.
Two pieces of news caught my eye today; a new mushroom has been described and named, and Sonic the Hedgehog, a video game character is 20. Read on to find out what the connection between them is.
Opinions are divided, heated debates can be heard in science departments the world over, the bone of contention? Should new genes, species, disease and other discoveries be named in an orderly fashion, or at the whimsy of the discoverer?
The privilege of naming a new discovery has long been the reward for diligence and hard work. Immortalizing oneself or an admired contemporary was the traditional choice. But more imaginative choices have also been made.
One of my favourites, and close to my heart, are the members of the hedgehog gene family. The first Hedgehog gene was discovered in 1978 by Christiane Nüsslein-Volhard and Eric Wieschaus, in the fruitfly, Drosophila. If Drosophila lack the gene for Hedgehog, they have a thick coat of spikes (called denticles) that reminded the scientists of a hegehog, and so that’s what they named it. Later, similar genes were found in vertebrates, but instead of there being just one Hedgehog gene, there were multiple, and they needed to be distinguished from each other, two were named after hedgehog species, Indian and Desert, whilst the most famous (and most biologically active) was amusingly named Sonic, after the video game character.
Fruitfly genes provide fertile ground for interesting names, such as the two mutants amnesiac and cheapdate. They’re both have defects in the same gene (called amnesiac), whilst the mutant amnesiac has memory loss, the change that causes the cheapdate phenotype (physical manifestation of a gene), lowers the fly’s tolerance to alcohol.
Other favourites are; methuselah, which increases the lifespan of flies, named after the biblical figure who lived to 969, stargazermutants look up over and over (due to an affect on the cerubelum) and brainiac flies have much larger brains then normal.
Zebrafish gene names are often imaginative too, such as the class of blood mutants, that were discovered by the Zon lab, which are named after fine wines, such as chardonnay, chablis and merlot (rumour has it that the discoverer of a new gene in the lab is awarded a bottle of the corresponding wine – hence an increase in more obscure and expensive wines as time has gone on!)
Understandably perhaps, the penchant for amusing names in science seems be dying out, in favour of methodical, structured naming, saving doctors from having to give the unfortunate news, for example, that a patient has a mutation in swiss cheese (which results in holes in the brain, although for the record, I know of no patients that have this mutation!)
However, wit amongst scientists has not been lost forever, for today I learnt of a new species of mushroom, discovered by researchers from
San Francisco State University,
that is shaped like a sea sponge, and was therefore named:
after the yellow-marine dwelling-cartoon character.
This makes me happy.
Caroline Parkin is a researcher based in the MRC Centre for Developmental and Biomedical Genetics at the University of Sheffield. She has her own website on the use of zebrafish as model organisms www.fishforscience.com
Dominant and Recessive Genes In Humans
As briefly referred to in the previous Genetics blog, for each of our genes we posess two ‘alleles’. One of these alleles in inherited from our father and one from our mother. There can be many different alleles for one gene and it can be completely up to chance, or perhaps luck, what we inherit from our parents. When speaking in general terms about dominant and recessive alleles, we tend to speak about genes as if for each of them there are two different alleles. This is not always, or often, the case, but it sometimes is and makes it much easier to explain this way.
For example, for a particular gene, say the ability to roll your tongue, there is a dominant and a recessive gene. We can call the dominant allele ‘R’ for being able to roll our tongue and the recessive allele ‘r’ for being unable to roll our tongue. Our parents could posess any combination of these alleles: AA, aa or Aa. Then, it is completely down to chance what we inherit from them.
One unexpected example is that the allele for dwarfism in humans is the dominant allele and the allele for normal growth is recessive. This means that if we inherited both of the different alleles for this gene we would show the dwarfism trait.
Below is a table of dominant and recessive traits shown in humans.
|
Dominant Trait in Humans |
Recessive Trait in Humans |
|
A blood type |
O blood type |
|
Abundant body hair |
Little body hair |
|
Astigmatism |
Normal vision |
|
B blood type |
O blood type |
|
Baldness (in male) |
Not bald |
|
Broad lips |
Thin lips |
|
Broad nose |
Narrow nose |
|
Dwarfism |
Normal growth |
|
Hazel or green eyes |
Blue or gray eyes |
|
High blood pressure |
Normal blood pressure |
|
Large eyes |
Small eyes |
|
Migraine |
Normal |
|
Mongolian Fold |
No fold in eyes |
|
Nearsightedness |
Normal vision |
|
Rh factor (+) |
No factor (Rh -) |
|
Second toe longest |
First or big toe longest |
|
Short stature |
Tall stature |
|
Six fingers |
Five fingers normal |
|
Webbed fingers |
Normal fingers |
|
Tone deafness |
Normal tone hearing |
|
White hair streak |
Normal hair coloring |
When we are speaking about the inheritance of alleles and the genetic make-up of a person with respect to one gene, we use one of two phrases. The first is homozygous, meaning that the two alleles an individual posesses for one gene are the same i.e. AA or aa. The second is heterozygous, meaning that the two alleles an individual posesses for one gene are different i.e. Aa.
By Robyn Bradbury
Blood Groups Could Become a Thing of the Past
Written by Matt Farley
New research from McGill University in Canada could do away with the need to classify blood by ‘type’, following a new technique to prevent mismatched blood from being rejected after a transfusion.
Along with the well-known A, B and O blood groups, there are a further 26 different blood types which have to be matched carefully when carrying out a blood transfusion – a mismatch can lead to the donated blood being rejected by the body which can be fatal. The ideal situation is for a ‘universal’ blood type which would be compatible with any recipient blood type.
Rejection occurs when the antigens on the surface of the donor red blood cells are of a different type to those on the recipient’s cells – previous attempts at avoiding this have focused on either removing the surface antigens from the donated blood using enzymes, or producing the blood outside the body from stem cells. These techniques have shown some success, but are hindered by their expense and complexity. The latest method, presented by Dr. Maryam Tabrizian and colleagues, instead aims to cover up the antigens and hide them from the host immune system – known as ‘immunocamouflage’.
Red blood cells from a selection of volunteers were coated in a layer of polyelectrolytes – small repeating units which self-assemble on the cell surface. Previous attempts at coating cells in this way using yeast and E.coli had shown promise, but it remained to be seen whether the delicate red blood cells would be able to withstand the process.
After coating, the cells were exposed to their opposite antibody and observed for any agglutination, or clumping of cells, that occurred. The coated cells were shown to remain free after addition of the antibody, suggesting that the antibodies had failed to recognise and bind the cell surface antigens. This was in contrast to the uncoated cells, which clumped together in the manner normally seen when mismatched blood samples are mixed.
Perhaps most importantly, the red blood cells showed no significant reduction in their ability to take up oxygen, implying that they would still be able to carry out their function within the body. The cells were also seen to produce ATP, an energy carrier – a good sign that metabolism was also functioning as normal.
It remains to be seen whether the technique will be as effective when tested in a living organism, but the results obtained so far appear promising. If effective, future blood transfusions could become a lot easier, and a lot less dangerous.
The paper accompanying this article is available online:
http://pubs.acs.org/stoken/presspac/presspac/full/10.1021/bm101200c
Red blood cells
Losing DNA made us human
Written by Olivia O’Sullivan
A study has shown that it may be DNA we have lost which sets humans apart from our nearest primate relatives.
The majority of mutations in DNA are harmful, and a loss of genetic information might be assumed to be catastrophic. In a paper published last week in Nature, a team of researchers from Stanford University in California have challenged this by identifying the loss of particular regions of non-coding DNA to be a key factor in shaping our unique minds and bodies, thus setting us apart from chimpanzees and the rest of the animal kingdom.
By conducting a genetic comparison of the human genome with that of a chimp and a macaque the team found 510 DNA sequences missing in humans that were present in chimps, almost all of these sequences were from the non-coding region of DNA, i.e. chunks of DNA responsible for turning genes on or off . Two regions of particular interest were the androgen receptor (AR) gene and ‘GADD45G’ – a tumour suppressor gene involved in brain development.
The AR gene is implicated in the production of hard, keratinized penile spines which are found in many mammals and play different roles in different species. It is thought that penile spines may have been used as a way of competing with other males for mating partners by removing the sperm of competitors. It is believed that the molecular changes resulting in a loss of human penile spines has allowed us as a species to form more complex social structures by adopting monogamous reproductive relationships.
Another ‘lost section of DNA’ in humans was found to code for a tumour suppressor gene that normally acts to suppress brain growth, putting an evolutionary brake on the growth of specific brain structures zones in our primate relatives. This ultimately paved the way for the evolution of a larger human brain, giving us an intellectual edge over our fellow animals.
The results of this study certainly underlines the fact that genetic information is both gained and lost during evolution and that despite sharing approximately 96% of our DNA with chimpanzees, it is thought that this genetic divergence may have occurred more than 800,000 years ago when our ancestors split from the Neanderthal lineage. This is an exciting finding, opening up new areas for discovery through the analysis of the remaining 508 DNA sequences which promise to reveal further secrets about the molecular basis of human individuality.
References:
McLean, C. Y. et al. Nature 471, 216-219 (2011)
Increased Solar Activity, how will it affect me?
Over the past month it has been reported that several large solar flares (or coronal mass ejections) have sent a mass of charged particles in the towards us indicating that after an extended period of relatively low activity, the sun is beginning to ‘wake up’. Accompanying these reports in the tabloids have been the generic sensationalist stories saying that the sun is going to let out the ‘big one’ and wipe us all out be it through the amount of charged particles hitting the Earth inflicting a high level of radiation upon us or that these will cut all of our electricity and we will be thown back into a pre 20th century darkness. Not only have the tabloids been jumping on the end-of-the-world-due-to-a-solar-flare scenario, films such as 2012 and ‘the knowing’ have used this as a major storyline. However, how much truth is in these stories and films? What will increased solar activity mean to you and I?
1. Satellites
Solar flares occur from a release of stored magnetic energy from sunspot activity, as a result charged particles are thrown out into space. These charged particles can affect and potentially shut down some of the many satellites orbitting the Earth having a profound affect on the way we go about our general day to day tasks. Understandably the different types of satellite such as, navigation, military, communication will effect different people in different ways. Periods of high solar activity occur on average every 11 years, the last time there was a peak the world was a very different place and we weren’t so dependent on technology. With this in mind we can only make predictions on smaller storms as to how badly solar flares will affect our satellites, and with these smaller flares being taken into account some of the predicted damage may not be so great. It’s understandable that some satellites may go down but newer ones should have precautions incase of these flares. So for how this will affect us we can initally say that the impact may not be that great but may mess up our satellite tv or our sat navs forcing us to use a map!
2. Communications
Following on from the effects caused by solar flares to satellites a major associated issue that could arise under the events of large scale solar flares is that of our communication systems ‘going down’. A loss of satellite communications can eliminate some pathways to communication around the world and the communications received as a result of satellite TV. Large solar flares and the stream of charged particles that emanate from them can also have an effect with long range radiowave communication as well. Communications that use the atmosphere to transmit over large distances can sufffer large amounts of interference due to extra charges and energy in the atmosphere. This also can apply to mobile phone communications that use microwaves to transmit data. It was also reported in the solar maximum in the 1970s that long range telephone communications were brought down by a solar flare in Illinois, US showing the effect that flares can have on facilities that are based on earth as well as in space.
3. Electrical Grids
In the last solar maximum, Quebec in Canada was hit pretty bad by a solar flare and as a result six million of it’s inhabitants were plunged into darkness as the power grids were affected. Understandably back in the 80s this caused a problem however it can be expected that if this occurred in the next solar maximum it will affect us a lot more due to our greater reliance on electricity in a gadget driven world. This will cause turmoil not only in the home but potentially businesses as well, as computer systems and communication lines go down due to a loss of power. This overall can also have a major affect on the economy.
…and finally a good one
4. Aurora
Aurora (otherwise known as Northern/Southern Lights) occur as charged particles emitted from the surface of the sun come into contact with the magnetic field around the Earth. They get trapped in regions known as the Van Allen belts which ‘focus’ particles towards the poles leading to the areas in Scandinavia for example where the Aurora occurr. The charged particles interact with Oxygen and Nitrogen in the atmosphere which through excitation and relaxation of molecules/atoms lead to the characeristic red and green glow of the Aurora. With increased solar activity comes increased Aurora ativity which when intense can happen further south, as a result more will have the opportunity to see this sight.
All in all, we will not be wiped out by a solar flare in the coming years as some would like to believe, however it is aparent that some measures need to be taken in order to lessen any damage to technology and the economy on Earth. Measures have already been taken to protect satellites so hopefully with measures taken to protect power grids the coming storm will cause us less trouble than it has the potential to deal out. And even if we are all plunged into darkness, at least light pollution won’t get in the way of the Aurora!
http://www.youtube.com/watch?v=GX_hoYYR3E4 there’s also an excuse to post a song I like called Solarwinds
What? A molecule that enables hearing
By Kathryn Vaughan
Researchers at the University of Sheffield have identified a molecule that underlies mechanisms of hearing loss and deafness.
In the inner ear ‘cochlear hair cells’ are responsible for receiving sound as sensory information before it can be converted into electrical nerve signals to be sent to the brain, and these hair cells mature during embryonic development. To examine the mechanisms that regulate cochlear hair cell maturation, researchers led by Walter Marcotti from the University of Sheffield have investigated the role of a molecule named miR-96. The molecule miR-96 is a microRNA, a short genetic sequence that regulates the expression of a range of genes, and is itself highly expressed in developing cochlear hair cells.
Mice that do not express miR-96, referred to as ‘knockouts’, were compared with control mice that do express miR-96. To examine differences in structure, hair cells from the two groups of mice were observed under a microscope and measurements were taken of both cell length and sensitivity to a neurotransmitter. By placing a speaker 20cm directly in front of each mouse and recording a ‘Preyer reflex’, whereby a mouse flicks its ear in the direction of sound, the researchers also measured auditory brainstem responses, which reflect the activity of the hair cell.
The researchers found that the cochlear hair cells of the mice that do not express miR-96 were thinner, shorter in length and more immature when compared to hair cells of control mice, identifying a role for miR-96 in the maturation of cochlear hair cells. To investigate the activity of the hair cells by measuring the auditory brainstem responses, the knockout mice could not be used since they have no auditory response at all. Instead, mice with limited miR-96 expression were compared with control mice and were found to be less responsive, indicating a defect in their hearing due to the limited miR-96 expression.
Measurements were also recorded to examine the sensitivity of hair cells to a neurotransmitter called acetylcholine. Acetylcholine is a molecule released from nerve endings and can act upon cochlear hair cells to initiate the conversion of an auditory response into an electrical nerve signal. Sensitivity to acetylcholine was reduced in knockout mice whilst control mice responded as usual, implicating miR-96 in hair cell activity.
These results indicate that in the maturation of cochlear hair cells, which is vital for the fundamentals of hearing, miR-96 plays an essential role. By understanding these mechanisms the researchers propose that the research “could provide us with clues to help develop therapies to ameliorate the effects associated with nonsyndromic progressive hearing loss”.
Cochlear hair cells in a Guinea Pig
References:
Kuhn et al (2011) miR-96 regulates the progression of differentiation in mammalian cochlear inner and outer hair cells. Proc Natl Acad Sci USA, 108 (6), 2355-2360.
The paper can be found at: