Science of the bloody brain

mosso 300x205 Science of the bloody brain

One of Mosso’s experiments. Each of the four traces on the right compares brain blood flow (red) and pulsations in the feet (black) simultaneously, during 1)resting 2)listening to the clock and church bells 3)remembering whether Ave Maria should have been said and 4)’8×12’?

Luigi Cane literally had a hole in his head. A brick had unforgivingly fallen on the back of it, smashing a section of his skull like a spoon knocking the shell off the top of a hard-boiled egg. And so, after surgery, part of the surface of his brain was left precariously unprotected except for a layer of skin. Peering through this accidental window into his head, Dr. Angelo Mosso was able to measure the pulsations of the brain’s blood supply. Cane sat in Mosso’s lab with pressure gauges strapped around his feet and a handmade instrument resting delicately on the skin over his vulnerable brain. This was to be the world première of neuroimaging.

972 Science of the bloody brain

Angelo Mosso, a 19th century physiologist and first brain imager

“What is 27 times 13?” Mosso inquired. Cane thought deeply and silently while the various contraptions simultaneously showed his feet shrinking while his brain swelled with blood flow. This experiment was the first to reveal that when our mental ‘cogs’ turn, a boost of blood is directed to the brain. Mosso confirmed this in individuals with intact skulls with what was essentially a wobble-board bed. When people lying down on the balance thought about tricky or even particularly emotional questions, it would tip down towards the head end with the weight of the extra blood.

The brain is an extremely greedy part of the body when it comes to blood. While it only makes up about a fiftieth of the body’s mass, it consumes up to a fifth of the total energy and oxygen carried in the bloodstream. Charles Roy and Charles Sherrington later proved that the blood rushing to the head was actually being diverted specifically to the parts that were most active – like a bonus for the busiest brain cells. Over twelve decades later, neuroscientists are still using this same principle to observe brain activity and the accompanying ‘rush of blood’ to the head.

The brain imaging technique functional magnetic resonance imaging (fMRI) works on the principal that deoxygenated haemoglobin (the protein that carries oxygen in red blood cells) has magnetic properties. In essence, fMRI can measure how well-oxygenated or deoxygenated different parts of the brain get when the person in the scanner performs a task, for example reading, writing, or thinking about chocolate. But information collected from this kind of experiment needs to be handled very carefully.

Face recognition Science of the bloody brain

Computer-enhanced fMRI scan of a person who has been asked to look at faces. The image shows increased blood flow in the part of the visual cortex that recognizes faces.

Firstly, fMRI is not a direct measure of brain activity per se; rather, it’s the triggered oxygenated blood flow response to brain activity. Secondly, no one really knows what a larger blood flow response means, especially in parts of the brain that have several jobs. Lots of blood in a specific part of the brain while doing sums might mean that a person can do sums easily because their blood supply is so efficient. Alternatively, it could be interpreted as suggesting that person struggles with mental arithmetic and needs more blood in their head to cope. Thirdly, fMRI data needs to be stringently tested to avoid seeing activity that isn’t there. Researchers at the University of California found that using different statistical tests they could see a blood flow response in the brain of a dead salmon while it was looking at different human faces – and won an IgNobel Prize for highlighting the dangers of shoddy stats.

With all this to bear in mind, it’s perhaps unsurprising that poorly carried out fMRI experiments have been dubbed the modern phrenology – the practice of comparing measurements of peoples’ skulls to infer personality traits. What is perhaps more surprising, though, is that despite the speculations on the validity and accuracy of fMRI, it is being used for things besides its more traditional remit. ‘No Lie MRI’ is a company in the U.S. that advertises the use of brain imaging to detect liars or untrustworthy individuals, whether they be potential politicians, investments or romantic interests. Brain imaging techniques including fMRI have even controversially been used as evidence in Indian courts of law.

pain 300x80 Science of the bloody brain

Example of fMRI responses to painful heat to the forehead in a cohort of 12 subjects. ACC, anterior cingulate cortex; PCC, posterior cingulate cortex (Moulton et al., unpublished observations). Borsook et al. Molecular Pain 2007 3:25

There are, however, other emerging uses for fMRI that may improve its reputation. By watching live feedback of the blood flow going to the anterior cingulate and insula, two pain centres deep within the brain, sufferers of chronic pain can consciously train these parts of the brain to receive more blood. Christopher deCharms and his colleagues at Omneuron have found that people who were given the real, live feedback from their insula and cingulate and successfully learnt to train the blood flow within these parts said they experienced less pain than usual. Conversely, people unwittingly shown a dummy feedback (random fluctuations or blood flow levels from an unrelated part of the brain) didn’t report any substantial pain relief.

Brain imaging techniques that rely on measuring blood flow around the brain should be carefully interpreted; fMRI is heavily-used in research and is still fashionable in brain research. Technology has come on a massively long way since the days of wobble boards, so we should probably count ourselves lucky that we don’t need a hole in our heads to unlock the further mysteries of the blood in our brains.

Post by Natasha Bray

 

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Hope for new MS drug which could repair damaged cells.

Researchers from the private biotech firm ENDECE Neural have just announced the development of a new compound they believe may have the potential to repair damage caused by multiple sclerosis (MS).

MS is the most common neurological disorder affecting young adults in the western hemisphere. Although scientists are still unsure of what causes the disorder, it is known that symptoms stem from damage to the fatty covering surrounding nerve cells, known as the myelin sheath. It is believed that in the early stages of the disease the body’s own immune cells (cells usually primed to seek out and destroy foreign agents within the body, such as viruses and parasites) mistake myelin for a foreign body and launch an attack. Since myelin is essential for fast neural communication and cell protection, the symptoms of MS stem from a slowing of neural communication and ultimately nerve cell damage.

oligo 253x300 Hope for new MS drug which could repair damaged cells.The myelin surrounding cells in the brain and spinal cord is provided by cells called oligodendrocytes. These cells reach out a number of branching arms which wrap around segments of surrounding neurons, forming the myelin sheath. The majority of drugs available for treatment of MS aim to reduce initial damage to this sheath. However, researchers from ENDECE are now investigating treatments which can increase the number of oligodentrocytes in the central nervous system, thus leading to remyelination of damaged cells. Dr. James G. Yarger, CEO and co-founder of ENDECE notes, “For decades, researchers have been seeking ways to induce remyelination in diseases such as MS that are characterized by demyelination,”. And now this dream may be becoming a reality.

ENDECE’s work revolves around their pipeline drug NDC-1308. Although the name isn’t likely to turn any heads, its properties just might. Following the observation that pregnant women typically do not experience the symptoms of MS during their third trimester, a number of researchers have been exploring a possible role for estrogen in the treatment of MS. ENDECE researchers created 40 separate estradiol analogues (substances similar in structure to estradiol but with a range of key modifications) and assessed their biological effects. From this work they found that one analogue (NDC-1308) had a particularly potent effect on oligodentrocyte precursor cells (OPCs – cells with the ability to become mature oligodentrocytes), causing them to differentiate into mature oligodendrocytes. In follow-up studies researchers found that treatment with NDC-1308 led to remyelination in a mouse model of MS, specifically showing a 20% increase in myelination in the hippocampus (a region of the brain known to experience demyelination in this model). NDC-1308 was also found to cause remyelination in the rat and to induce cultured OPC cells to differentiate into mature oligodendrocytes. Taken together, these findings suggest that NDC-1308 may prove effective in restoring the lost myelin sheath on damaged axons in patients with MS.

Dr. Yarger states, “We envision NDC-1308 being administered either alone or in combination with current therapeutics that target the immune response and/or inflammation associated with MS. By inducing remyelination, it may be possible to restore muscle control, mobility, and cognition in patients with MS. Therefore, a drug that induces remyelination, such as NDC-1308, can potentially double the size of the current market for MS therapeutics.”

NDC-1308 is still in late preclinical development, and has yet to go through rigorous safety screening and clinical trials. However, as a drug that potentially stimulates remyelination, it represents a whole new strategy for the pharmaceutical treatment of MS patients in the future.

Post by: Sarah Fox

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Cancer resistant rodents – the naked truth

The naked mole rat is a quirky little creature. These mouse-size rodents may be curious-looking, but they are fast becoming the rising star of cancer and ageing research. Their unusual lifestyle alone makes them interesting – unlike any other known mammal, mole rats are eusocial. They live in large underground colonies, forming a social structure more akin to a hive of beesmolerat 300x199 Cancer resistant rodents   the naked truth than any rodent species. The colony centres around a single female, known as a queen, who mates with a handful of fertile males. The rest of the colony, which can consist of over 80 individuals, are infertile workers.

The scientific interest in naked mole rats stems from a number of intriguing observations; firstly, the naked mole rat can live for up to 30 years, around ten times longer than a mouse or rat. In fact, relative to body size, if humans were to live as long as these little guys it wouldn’t be uncommon for us to reach our 600th birthday! Equally fascinating is the fact that these animals never appear to suffer from cancer. Long term studies of naked mole rat colonies have consistently failed to find any incidence of naturally occurring tumours in these lucky rodents.

But there’s more than luck involved in this process. Research suggests that a specific adaptation, which originally evolved to make these rodents more manoeuvrable in tight spaces, also gives naked mole rat cells some serious personal space issues. Their cells never divide to the point of overcrowding (a process necessary for tumour development). This gifts the mole rat with resistance to cancer.

But how is this possible?

Researchers from the University of Rochester in New York have found that mole rat cells make a unique ‘gloopy’ polysaccharide known as high-molecular-mass hyaluronan (HMM-HA) which is released from specialised cells called fibroblasts. This substance is similar but much larger than human, mouse or guinea pigs (one of the mole rat’s closest relatives) hyaluronan. When hyaluronan comes into contact with cells it causes a range of reactions, the nature of which depends on its size. High-mass hyaluronan stops cells from dividing and also shows anti-inflammatory properties, whereas low-mass hyaluronan has the opposite effect. Thus, the properties of high-mass hyaluronan may explain why cultured mole rat cells are much more ‘anti-social’ than those from other mammals, preferring to grow at a lower density than tissue from mice, humans or guinea pigs.

molrrat4 300x225 Cancer resistant rodents   the naked truth

We love you naked mole rat! (this little guy is certainly on my Christmas list – http://tinyurl.com/nttn6gq)

It was also found that mole rat cells are resistant to manipulations which would lead to tumour growth in other mammals. However, if HMM-HA production is reduced in mole rat cells then tumours are able to form. This indicates that the interaction between HMM-HA and the cell is vital for tumour resistance.

Scientists are now investigating how HMM-HA instructs cells to stop dividing. It is hoped that in the future an understanding of these mechanisms may open new avenues in the field of cancer prevention and life extension. So perhaps the enigmatic, awkward looking, naked mole rat is proof that beauty really is only skin deep!

Post by: Sarah Fox

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Do infections speed up memory loss in Alzheimer’s?

How does an infection affect the progression of Alzheimer’s disease?

Microglia and neurons Do infections speed up memory loss in Alzheimer’s?

Microglia (green) and neurons (red) living in harmony…for now. Image by Gerry Shaw, EnCor Biotechnology Inc. (Wikicommons).

Alzheimer’s disease (AD) is the most common form of dementia. It’s a neurodegenerative condition characterized by ongoing cognitive decline, loss of functions such as memory, and behavioural abnormalities. AD usually occurs amongst the elderly, and its prevalence is now so high, that its estimated overall cost to society is 5 times that of cancer, heart disease and stroke. While AD was first identified over a century ago, research into its causes has only really begun to gather momentum over the past 30 years. Some think that damage may stem from the formation of toxic ‘plaques’ and ‘tangles’ that appear to be associated with brain cell death. Unfortunately, understanding the triggers of neurodegeneration has become a much more troublesome challenge.

Some teams have begun to look at the contribution of inflammation to the development of brain atrophy (shrinkage). Inflammation is the first response of the immune system to infection/injury. You can recognise inflammation when you graze your skin or sprain an ankle: as well as pain, there may be redness, swelling and the area may feel hot to the touch. This is thanks to the extra blood carrying immune cells to the site of injury to prevent infection and aid repair. The inflammatory response is an innate and usually protective reaction to injury or infection and requires the co-operation between local, ‘resident’ immune cells at the site of injury and circulating immune cells in the bloodstream.

Hippocampus Do infections speed up memory loss in Alzheimer’s?

The hippocampi (red) as seen from below the human brain, looking up. (Image from Wikicommons).

The main resident immune cells of the brain are called microglia; they respond to infection and injury to trigger an inflammatory response. Microglia are hyper-sensitive to changes in their local environment. When the brain is injured, they become ‘activated’. They change shape and behave differently, releasing different chemicals which can be toxic to brain cells. Some research has suggested that it’s possible that activated microglia break down the connections between cells in the memory centre of the brain, the hippocampus. Intriguingly, hippocampal damage and memory loss are the primary symptoms of AD.

Several lines of evidence have implicated microglial inflammation in AD, including the observation of activated microglia in the brains with Alzheimer’s, and the possibility that anti-inflammatory drugs may be neuroprotective. However, clinical trials have failed to show any efficacy yet.

Professor Hugh Perry and his research group at the University of Southampton investigate how inflammation contributes to outcome of brain diseases. About ten years ago Perry and his team developed an animal model (the prion mouse) to better understand the complex role of inflammation in AD. A chemical that causes neurodegeneration was injected into the mouse hippocampus (the memory centre of the brain), and the researchers studied the evolution of the resulting prion disease, which bears some similarities to AD. Thirteen weeks after the injection, although the mice appeared normal, there were more activated microglia found in the hippocampus, even compared to surrounding areas of the brain. The researchers then claimed that this microglial activation was pathological, since the mice showed some behavioural disturbances and deficits in learning tasks.

Perry and his team suggested that systemic infections in patients with AD could worsen cell death in the brain, speeding up neuron deterioration and memory loss. (‘Systemic’ infections are so-named because they infect a number of organs and tissues or affect the body ‘system’ as a whole, instead of being localized in one area.)

Mikroglej 1 Do infections speed up memory loss in Alzheimer’s?

Makrofagi 2 Do infections speed up memory loss in Alzheimer’s? Resting (top) and activated (bottom) rat microglia after a brain injury. Images by Grzegorz Wicher (Wikicommons).

To look into this idea, researchers looked at differences between the prion mouse with an ‘infection’ (or rather, an injection of a toxin released by bacteria to mimic an infection) or without infection. The prion mouse given a fake infection had twice as many dead brain cells as the uninfected prion mouse. Researchers concluded that the microglia are primed by the ongoing prion disease and so, when the infection is added, they overreact. They then drive the production of a number of inflammatory chemicals, which triggers a whole host of damaging effects on brain cells.

Perry and his team collaborated with other research groups to identify whether the evidence they had gathered would be relevant to AD patients. In a small pilot study of 85 AD patients with moderate cognitive impairment scores over 2 months, they found that those who had infections showed a more cognitive decline than the other patients in the study. This was the first evidence in a clinical setting that systemic infection may affect neurological disease progression. The next study involved 300 AD patients, 50% of whom had a systemic infection within the recorded 6 months. The researchers saw that patients that got an infection within the 6 months suffered three times the rate of cognitive decline, compared to a small cognitive decline in those who had not had an infection.

These fascinating studies have provided the first clinical evidence that as well as inflammation in the brain driving damage, infection and inflammation in the body can also worsen and speed up neurodegeneration. It appears that brain-resident microglia become primed for activation, so that when patients suffer from a bodily infection, their brain cells become more vulnerable to the damaging effects of an inflammatory response.

Not only did this research provide ideas to potentially help AD patients today, but it also formed the basis for an important direction for current disease research. The evidence on the highly complex interplay between the diseased brain and systemic inflammation can be applied, not just to AD, but as a generic concept to many nervous system diseases.

Post by Isabelle Abbey-Vital

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Hating greens and “taster” genes: the bitter truth

sprouts Hating greens and “taster” genes: the bitter truthYou’d be hard pushed nowadays to find anyone unaware of the “five-a-day” rule surrounding fruit and vegetables in our diets. Green vegetables, in particular, are associated with numerous health benefits, such as reduced risk of coronary heart disease.1 Yet consuming enough of these foods on a daily basis can be hard, especially if you find greens like Brussels sprouts unpleasantly bitter. But why do some of us find these vegetables less palatable? And can anything help make sprouts more appetising? Scientists in the fields of genetics and food science (or bromatology) are working to find the answers.

We all carry a unique set of instructions within our genes, defining who and what we are. Our genes encode the protein building blocks that form our bodies, including protein receptors (or sensors) within our taste buds. These receptors interact with food passing through our mouths telling us how bitter, salty, sweet, sour or umami it tastes. A special group of genetically determined receptors, known as the TAS2R group, detect bitter tastes, meaning that our genes play a key role in determining how bitter our food tastes.

The genetics behind bitterness is complex, but scientists have established a common test to explain why some people experience certain foods as being more bitter than others. This test involves the TAS2R38 bitter taste receptors and two substances they detect, phenylthiocarbamine (PTC) and 6-n-propylthiouracil (PROP). In general, the functionality of a person’s TAS2R38 receptors determines to what degree they taste PTC or PROP as bitter, with people being divided into three groups: non-tasters with non-functional TAS2R38 receptors (PTC and PROP do not taste bitter), medium tasters (PTC and PROP taste slightly bitter) and “super tasters” (PTC and PROP taste very bitter).2,3 But what does this have to do with green vegetables?

yuck Hating greens and “taster” genes: the bitter truthIn 2006, a lab group from Yale and Connecticut Universities set out to investigate PROP as a marker for bitterness in green vegetables (Brussels sprouts, kale and asparagus) and whether this related to peoples’ intake and preference. 110 individuals were asked to rate these vegetables, along with PROP, for bitterness and likability whilst also being asked to complete a questionnaire regarding their daily diet.

Interestingly, the results showed that people who tasted PROP as most bitter (i.e. super tasters) also found the green vegetables very bitter, inferring PROP could be a marker of bitterness for this food group as well and suggesting TAS2R38 receptors may be involved in green vegetables’ bitterness.2 These people also tended to dislike greens more and eat less of them, suggesting a strong (and logical) relationship between a food’s bitterness and a lack of it in one’s diet. Thus, it seems for super tasters our genetic predisposition to produce functional TAS2R38 receptors may be working against us getting our five a day; making us find green vegetables bitter and unpalatable.

But all is not lost! Food scientists are now working on a solution to the super taster’s quandary. Mastaneh Sharafi and colleagues from the Allied Health Sciences Department at Connecticut University recently investigated the use of additives (aspartame, sodium chloride and sodium acetate) in a pilot study aimed at reducing or ‘masking’ green vegetables’ bitterness. Sharafi began by grouping 37 participants into non-, medium and super taster groups using PROP. They were then asked to rate plain and bitter green vegetables (asparagus, Brussel sprouts and kale), served together with one of the above masking agents, for likability.

To the researchers surprise, it seemed the masking agent’s effectiveness differed depending on both the vegetable and whether participants were non-, medium or super tasters. For super tasters, for instance, the two salt solutions reduced bitterness in asparagus but not sprouts or kale. Aspartame decreased bitterness across all the vegetables for super and medium tasters but had no effect for non-tasters. Participants with a significant dislike of greens and subsequent lack of these in their diets, reported improved likability with aspartame, suggesting masking agents could be useful to increasing green vegetable intake in disinclined individuals.3

So, it appears green veg haters can take some comfort in knowing that their dislike of sprouts is more likely due to their genetics than a desire to be difficult at dinnertime. And that masking these unpleasantly bitter tastes may hold the key to a palatable and balanced diet. Shafari’s small, yet noteworthy experiment certainly shows good prospects for aspartame and salt-based masking additives, but further work is still needed before us super tasters can comfortably achieve our “five-a-day”.

Guest Post by Megan Barrett

Megan is currently working as an associate writer at a medical communication company. You can follow her on Twitter @Meg_an12.

  1. Drewnowski A, Gomez-Carneros C. 2000. Bitter taste, phytonutrients, and the consumer: a review. Am J Clin Nutr. 72(6): 1424-35. http://www.ncbi.nlm.nih.gov/pubmed/11101467
  2. Dinehart M, Hayes J, Bartoshuk L, et al. 2006. Bitter taste markers explain variability in vegetable sweetness, bitterness, and intake. Physiol Behav. 87(2): 304-13. http://www.ncbi.nlm.nih.gov/pubmed/16368118
  3. Sharafi M, Hayes J, Duffy V. 2013. Masking vegetable bitterness to improve palatability depends on vegetable type and taste phenotype. Chem. Percept. 6:8-19. http://link.springer.com/10.1007/s12078-012-9137-5
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Excellent scientists that you probably haven’t heard of

There are some scientists that everyone has heard of; Darwin, Newton and Curie all spring to mind. Of course, their scientific discoveries were all legendary. But what about the people who have contributed just as much to the world of science but who maybe aren’t so famous? Here I’ve compiled a small list of some of the scientists I think have contributed just as much to our understanding of the modern world as those mentioned above. Although many of these people have been recognised in their fields and some have even won Nobel Prizes, their names have never entered the wider public consciousness.

1.       Rosalind Franklin (1920 – 1958) and Maurice Wilkins (1916  – 2004)

DNA 300x225 Excellent scientists that you probably haven’t heard of

The Structure of DNA. http://commons.wikimedia.org/wiki/File:DNA_Helix_CPK.jpg

Whilst Franklin and Wilkins are probably the best-known names on this list, they are not as well-known as they should be.  The discovery that DNA is a double helix is now forever associated with (James) Watson and (Francis) Crick. However, there were other names involved in this remarkable achievement, including Wilkins and Franklin who were working at King’s College London at the time of the discovery. Maurice Wilkins even shared the 1962 Nobel Prize with Watson and Crick, yet somehow his name has been lost from the public consciousness. His student was Rosalind Franklin, whose work with X-Ray diffraction was the key to confirming that DNA is indeed a double helix. Much has been made of Franklin not winning the Nobel Prize along with Watson, Crick and Wilkins. But, the sad fact is that the Nobel Prize is not awarded posthumously and by the time the discovery received this honourable recognition she had sadly passed away – at the tragically young age of 37. However, what I believe to be even more scandalous, is that her contribution seems to have been entirely overlooked until a few years ago when the deserved recognition began to flow in.

As for Wilkins, Watson himself states in his autobiography ‘The Double Helix’: “I proceeded to forget about Maurice, but not his DNA photograph”1. There is no doubt that the work done by Wilkins and Franklin was instrumental in aiding Crick and Watson with their ground-breaking discovery and their names certainly deserve to be remembered!

2.       George Gey (1899 – 1970)

Lamp1 copy 300x287 Excellent scientists that you probably haven’t heard of

HeLa Cells. Stained for lysosomes (green) and DNA (blue). Photo credit: Louise Walker, 2011.

Although he is a figure of some controversy, I think George Gey (pronounced “guy”) deserves to be on this list. Gey was the first person to propagate the HeLa cell line – the first human cells to be successfully grown in a laboratory environment. Since then, scientists have used HeLa cells, and other cell lines created since, to make many important breakthroughs, including the discovery of a treatment for polio. And they are still used in thousands of labs across the world, including mine (see picture).

The controversy surrounding Gey2 is the fact that the HeLa cells were taken from a cervical cancer patient, Henrietta Lacks, without her permission. Gey did not ask Henrietta or her family for permission to use or distribute the cells. The cell line was later patented and has made those who patented it (incidentally, not Gey or his family) very rich. Henrietta’s family received no money for the use of her cells, and until recently, Henrietta’s contribution went unacknowledged. George Gey however, did not have such financial motives; once he managed to successfully grow the HeLa cells, he gave them away to fellow scientists.

Whilst controversy remains as to how much money the Lacks family should be entitled to, I like to remember George Gey; the man who started it all out of altruism with no financial motives, a quality that should be admired.

3.       Sir Edwin Southern (1938 – )

Tsg101 blot 300x79 Excellent scientists that you probably haven’t heard of

A Western Blot. Showing the protein Tsg101 after elution from a gel filtration column, if you’re really that interested.
Credit: Louise Walker, 2011

Here’s one for fellow biochemists. Edwin Southern is a British molecular biologist and inventor of the Southern blot. This is a method for detection of DNA, now commonly used in DNA fingerprinting and genetic profiling. The Southern blot was later developed into the cleverly-named Northern Blot – modified to detect the other form of genetic material, RNA. Even better, the development of the Southern Blot finally led to development of the Western Blot – a method used to detect proteins. These methods are probably used by every biochemistry lab across the world, including mine (see picture).

The Southern blot and its offshoots have become staple practices in the lab and have made way for many important discoveries. Yet I know few biochemists who have even heard of Edwin Southern or his contributions to the scientific methods they use on a daily basis.

4.       Dorothy Crowfoot Hodgkin (1910 – 1994)

Insulin 300x231 Excellent scientists that you probably haven’t heard of

The Crystal Structure of Insulin Credit: http://commons.wikimedia.org/wiki/File:Insulin.jpg

Another British scientist, Dorothy Hodgkin, won the Nobel Prize in Chemistry in 1964 for discovering the structure of vitamin B12. She was a pioneer in the field of X-Ray crystallography, working on solving the crystal structure of proteins. Her knowledge was instrumental in the discovery of the structure of several proteins, but arguably her greatest achievement was in leading the team that solved the structure of insulin. This discovery led to the development of synthetic insulin – now widely used to treat people with type I diabetes.

Hodgkin has been recognised for her work in the scientific community. Along with the Nobel Prize she was also the first woman to win the prestigious Copley Medal. Some of her fellow recipients include Charles Darwin and Stephen Hawking. She was a true pioneer, not just for women in science but also for promoting peace and aid for developing countries. (According to her Wikipedia page, she did teach Margaret Thatcher, but I guess nobody’s perfect.)

While you could argue that most of these names are well-known in scientific circles, they have not become household names along with the likes of Darwin and Hawking. And this is by no measure an exhaustive list!

Perhaps one of the most endearing qualities of great scientists is that they rarely do what they do for fame or fortune. In fact, many actively shy away from the limelight. People like George Gey and Dorothy Hodgkin were certainly more interested in curing disease and adding to our understanding of the world than earning money or becoming famous. So this is just my way of thanking them for their tireless work and recognising the contributions they have made to modern science.

Post by: Louise Walker

1 The Double Helix by James Watson, Simon and Schuster, first published 1968

2To find out more about Henrietta Lacks and George Gey, see The Immortal Life of Henrietta Lacks by Rebecca Skloot, Pan MacMillan, 2011

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Attacked by your own hand: when the brain acts against you

Sometimes it might feel like your brain acts against your own interests. Who hasn’t regretted that extra pint or an unaffordable shopping spree? But what if your brain was controlling a part of your body against your will?

This is a relatively rare but mind-boggling condition called alien hand syndrome, where patients have the sensation of a limb acting without their control. It can feel like their arm is disobedient, and has “a will of its own”. The condition appears in the 1964 film Dr Strangelove, where the eponymous character is shown to have the condition. Medically, it was first documbetween the two hemispheres of the brain (the corpus callosum) cut. ented in patients who had undergone surgery to treat epilepsy, though it can occur after other types of brain surgery, stroke, brain tumours, infections or certain degenerative brain diseases. It is best understood in patients with epilepsy who have had the connection Following this surgery patients are generally able to continue their lives as normal, but in some cases the effects can be dramatic.

hand2 Attacked by your own hand: when the brain acts against you

Patients with alien hand syndrome report that following the surgery one arm (and sometimes leg) feels like someone else’s, and describe the arm’s behaviour as not their own. Some patients may even be unaware of the actions of their hand. One patient who suffered a severe case of alien hand syndrome and appeared in the 2011 BBC documentary “The Brain: a Secret History”, described how her “alien” left hand would take things out of her handbag without her knowledge, or stub out a cigarette that her right hand had just lit. In cases where the “alien” hand performs goal-directed behaviours such as these, it may perform actions directly opposed to the unaffected hand, leaving the hands apparently bickering. For instance, while the unaffected hand tries to pick up a mug, the other moves it away. Conversely, the affected hand may involuntarily mirror the actions of the other hand. For these patients, when instructed to perform an action with the unaffected hand, they may be unable to do so without the affected hand attempting the same movement. In another case, reminiscent of a horror film plotline, following serious heart surgery, a patient found that her left hand was no longer under her control, and would even try to choke her. Frighteningly she had to physically restrain it with her right hand to avoid injury.

So what is going on in the brain to allow this to happen? Brain imaging research has found that alien hand movements, like normal hand movements, are accompanied by activity in the primary motor cortex (a part of the brain critical to producing movements). But this occurs without the usual preceding activity in the premotor cortex (another part of the brain involved in planning and producing motor actions), and other regions involved in planning behaviours. In patients who have had the connection between the hemispheres cut, it is possible that interhemispheric premotor to motor cortex activity is disrupted. So, in effect, the motor cortex is acting without the usual sequence of brain activity that controls it and gives us a sense of the action being one we’ve chosen to do. In addition, in the healthy brain, motor actions are accompanied by a signal to the sensory parts of the brain that will experience it (an efferent signal; see an earlier post on this blog about how this stops us from being able to tickle ourselves here). If this efferent signal is absent or faulty, your own actions may feel like someone else’s.

brain Attacked by your own hand: when the brain acts against you

Although it is still not fully understood what changes in the brain lead to alien hand syndrome, it seems possible that a combination of these disturbances in the brain may contribute to the sensation of the hand being autonomous. This condition has fascinated scientists for many years, and raises interesting questions about how we experience physical sensations.

Post by: Claire Scofield

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