Mind the age gap!

Institutions need to rethink age and ageing

On 19 November, the Innovation Debate 2013 took place, concentrating on a topic that for many remains hard to face up to – the Age Crunch.

Life expectancies are continually on the rise. With every day we live, our life expectancy increases by 5 hours. Nowadays, many of us are expected to live well into our 80s, and in the UK, there are more people aged 60 and above (10.3 million) than there are under 18. But with society’s obsession with youth (e.g. Botox, anti-ageing treatments), we seem to have overlooked the challenges that come with an ageing society, such as pension plans and employment.

In a recent business survey,* 40% of employers stated that over-50s account for 25% or more of their workforce. It is expected that by 2020, a third of UK workers will be over the age of 50. Although business leaders appear to value their older workforce and 81% worry that skills will be lost when their older workers retire, only one in five employers (19%) sees keeping older workers as a priority.

Leading government advisor on ageing, Professor Tom Kirkwood, has warned that urgent action must be taken to preserve the mental capital of older workers; if not, the skills gap will only continue to grow. Baroness Sally Greengross, a crossbench member of the House of Lords, adds: “There is also significant denial around the implications and consequences of our rapidly ageing population in businesses and within our society as a whole… We need to change our attitudes and to stop defining age by the number of birthday candles we have on a cake.”

The likelihood of people being expected to work over the age of 65 is ever increasing, but what does the population think about working longer? Not much, it would appear – a third of those asked** would like to retire by the age of 60, although 45% don’t feel they have adequate provisions for their retirement.

Changes to employment and to pension schemes aren’t the only challenges an ageing population will face. It will also require adaptations to our current healthcare system. Professor John Appleby, chief economist at the King’s Fund, remains hopeful about the future, however: “Ageing is often framed in a negative light, seen as placing unsustainable pressure on health services. But in reality, its impact on NHS costs is less dramatic than might be assumed. Increases in life expectancy also extend the number of years of healthy life; so, rather than increasing healthcare costs per se, they tend to defer the costs associated with death. However, in order to cater better for the health needs of this changing demographic, we do urgently need to examine the way our care services are organised and funded.”

We will certainly hear more about the ‘Age Crunch’ in the coming years. Rather than seeing it as a burden, we could try to embrace the population shift as an opportunity for positive change for everyone.

(This article was published in the London Student)

Dreams – repressed desires or warning signals for disease?

This is an article I wrote for the London Student

Our fascination with dreams dates back centuries. Ancient cultures such as the Egyptians and Greeks even had dedicated gods of dreams. In the early 20th century, the founding father of psychoanalysis, Sigmund Freud, suggested that dreams are a manifestation of our most secret and repressed desires; and instead of living them in real life, we act them out in our dreams. Recent research has shown, however, that there might be more to dreams than just unfulfilled needs. In fact, dreams could be an indicator and predictor of certain diseases.

Nightmares, for example, could be a sign of heart conditions, migraine, sleep deprivation or a side effect of beta-blockers. Many dreams could be an indication for either being too hot or cold during the night, hormones, chronic pain, or coming off antidepressants.

Too much alcohol, an infection, the menopause or anti-malaria pills could cause memorable or bizarre dreams. A fatty meal, too much weight, stress or depression could give you dreams that wake you early; and sexual dreams do not necessarily represent anything about a person’s sex life, but could actually be triggered by creativity. Many pensioners reported having increased sexual dreams, which could be caused by taking up new hobbies during retirement.

Bashing about in your dreams, or dreams of attacks or wild animals, could be an early warning sign for Alzheimer’s or Parkinson disease. These dreams can be one of the first recognisable symptoms and can appear even a decade before the actual onset of the disease.

Alzheimer’s is a neurodegenerative disease, in which insoluble mutated protein (amyloid-β)clumps called plaques accumulate in the spaces between nerve cells. Protein tangles can even build up in nerve cells, thus hindering nerve cells to function properly.

Sleep disturbances, and in particular increased daytime sleepiness, could be an early sign of Alzheimer’s, which could be caused by the protein plaques. Researchers discovered that in mice the plaque concentration peaked during wake times, but fell when mice were asleep. Depriving mice of sleep increased the protein concentration dramatically. Once the plaques were removed, their sleep pattern went back to normal. Daily fluctuations in the concentration of the mutated protein were also found in humans.

It remains unclear whether the sleep disturbances lead to Alzheimer’s, or if they are caused by it, but it is suspected that they might reinforce each other. “Abnormal sleep in mid-life might cause protein aggregation that starts the disease off,” Holtzman tells Nature “, and the damage it causes may further disrupt sleep.” “Once we saw that amyloid-β was going up and down with the sleep–wake cycle, the implications began to unfold,” says Holtzman. These findings suggested that sleep disturbances might actually precipitate plaque formation. And if a sleep deficit could increase the concentration of soluble amyloid-β, says Holtzman, then sleep abnormalities in earlier life may predispose people to Alzheimer’s.”

During an 8-hour sleep period, the brain goes through different stages of electric activity in repeating cycles that change about every 90 minutes. We spend about 20-25% of our sleep in the REM phase (rapid eye movement), which is often associated with dreaming. During sleep, information is downloaded from one brain region to another, so sleep is a crucial time for learning and memory consolidation. It is now known that memory processing and even dreaming are not confined to the REM phase. It might help us, however, to deal with emotional processing of events that happened during the day. Research has shown that the slow wave sleep phase is very important for memory consolidation and learning, but it becomes shorter in the ageing brain. It seems that an ageing or deteriorating brain, bad memory and bad sleep are somehow connected.

Many factors can influence the sleeping and dreaming pattern, we can control some, but others we cannot. Despite a lot progress in research, our understanding of the brain and its functions remain partly unclear. Until we have resolved the mystery of why we dream, what our dreams mean, dreaming will certainly remain an enigma that will not cease to surprise and entertain.

Diaries of a wimpy teenage stem cell

I had a go at imaginative science writing:

Hello, I am Stemmy. I am a stem cell, and I am a superhero. As a stem cell, I have the power to develop into any other cell. This gives me the superpower to treat and maybe heal people suffering from diseases. I can remain a stem cell for a long time, or become any cell I want.

Sometimes it is hard to be a superhero. I have many brothers and sisters, and we all have the same superpowers. So what makes me unique? When other cells ask me what I am and who I want to be when I grow up, I have to say I am not sure yet. Except that I would like to be different from anybody else—I want to be special!

But on second thought, I guess I am quite special. I am a cord blood-derived stem cell, CB-SC, or as I like to say CB. I was collected from my human “donor” after his birth. Strictly speaking, some humans with white coats and facemasks collected my siblings and me from the blood inside the umbilical cord and stored us in freezers.

My stem cell family is very big. There are many types of stem cells depending from which part of the body they have been collected. There are the embryonic stem cells, collected from an embryo, the tissue stem cells, found in various body tissues, and the induced pluripotent stem cells (until recently, I didn’t even know they existed). Well, and there is us, the CBs. We all have slightly different superpowers, but I think that my sibling CBs and I are the coolest.

We actually go under several names, such as haematopoietic (blood) stem cells or HSCs, but I prefer CBs, or if you are just talking to me, please call me Stemmy. It is thanks to us and other HSCs from the bone marrow that humans know about stem cells; our discovery was the beginning of stem cell research. We are similar to embryonic stem cells, only that we don’t have quite as much potential; but we can divide into many different cell types, in particular blood cells. The white-coats are not quite sure about our superpower to develop into many different kind of cells, but it’s definitively certain that we can develop into any blood cell: white and red blood cells, and platelets. So OK, I might have exaggerated at the beginning, when I was bragging about my superpower to become any cell I want. I have to admit I was a bit jealous of my siblings, the embryonic stem cells.

Embryonic stem cells cause quite a bit of fuss, if you ask me. The reason for this is that they are harvested from an embryo that was specifically grown for that purpose–I know, that sounds crazy. But this means that after the stem cells are taken from the embryo, it can’t develop any further and grow into a human baby, which causes a huge debate among humans. Some people say, embryonic stem cells aren’t so cool, because of issues related to their harvesting, and because so far, they’ve “only” been used to cure diseases of the eye. If you ask me, I think the embryonic stem cells are pretty impressive–depending on when they are collected they can develop into any other cell of the human body. How cool is that! There are over 200 types of cells in the human body, so I think that's pretty amazing.

My other siblings are the adult stem cells and the IPSCs, short for induced pluripotent stem cells. Adult stem cells have less choice in becoming whom they want. They can be found in babies, children, or adults, usually in already developed tissues of the heart, brain, or kidney. An adult stem cell that lives in the kidney will usually create the same kind of cells; but it would have the potential to turn into many other types of cells too, just not 200.

The IPSCs, they’re a bit weird if you ask me. Actually, on second thought I am glad that I am not called IPSC, what a lame name. IPSCs are grown-up cells, but can be reprogrammed to kind of act as a stem cell. Because embryonic stem cells are not as easy to get hold of, and often, some people are a bit against the idea to grow embryos just to harvest stem cells, the white-coats have come up with another brilliant idea. What if they would take an adult cell, and try to reprogram it back to its origin? And that’s what they did, and guess what, they used some virus to do that, and even crazier, it worked. They tried it on skin cells, and managed to turn them into their original stem cell line! Obviously, that’s a huge success, because it will be a lot easier to get stem cells this way. But this technique is quite new, and the white-coats need to understand how exactly the IPSCs act, and if they’re really like embryonic stem cells. Yes, I admit it, I might be slightly jealous here too, because although IPSCs might not have much of a freedom to choose who they want to be, they might very well become famous because of their “x-factor”.

In a way, my big stem cell family is pretty cool. We can be used not only to create new cells or tissues, we can also help to test new drugs for diseases and help the white-coats understand how diseases come about and how they can be treated.

We recently heard that our cell donor, Sammy, had some bad news a few weeks ago. He has leukaemia, the poor fellow–a good thing that my siblings and I were collected at his birth. I guess I do have a purpose after all.

We are going to be mixed with Sammy’s blood and transform into blood cells to help him fight his disease. Yeah, I know, so much for freedom of the mind. I might not be able to make my own decisions after all, but if it helps Sammy, I would have chosen to be a blood cell anyway. And that way, my existence did have a good purpose! And I might even become famous. If the therapy is successful, we will be all over the news, and hopefully Sammy will be able to finish high school soon, and go to University. I heard that when he’s older, he wants to become one of those “white-coats”.

Well, so long, guys. Wish me luck on my mission to become a blood cell.

Lotti the snapper turtle

Since several weeks, the community of Irsee, Germany, has been “terrorised” by an alligator snapping turtle. It appears that the reptile has chosen a pond used for public swimming (Oggenrieder Weiher) as her new home; and allegedly bit through a boy’s Achilles tendon.

Although the community of Irsee has lovingly baptised her “Lotti”, I am sure that most of the people living in the “terrorised region” are far less appreciative and excited about this turtle than I am.

Snapping turtles are amazing creatures—they have walked with dinosaurs. Snapping turtles have evolved around 40 million years ago. They are very similar to the Proganochelys, the most primitive turtle that existed around 215 million years ago.

Individuals live between 50-100 years. Males measure around 26 inches (66 cm) in shell length and weigh about 175 pounds (80 kg). They have very good eyesight in and out of the water.

Snapping turtles like to fish! They have a bright red, worm shaped tongue, which they let float in the water to lure in fish and frogs.

Snapping turtles can still be found in North America, but they’re registered as a threatened species. They live in the water, but females crawl ashore to nest in the breeding season. There are two types of snapping turtles: the Common Snapping Turtle (Chelydra serpentina) and the Alligator Snapping Turtle (Macrochelys temminckii). Alligator snapping turtles have a spiked shell, a thick scaled tail, and their most impressive feature—beak-like jaws.

Back in Germany, after a few weeks of intensive search missions, live traps and a drained pond, there is still no sign of Lotti. Specialists are currently training a sniffer dog to search for Lotti.

It is still unclear how Lotti ended up in the pond. The import of Snapper turtles (into Germany) has been forbidden since 1999. Despite their looks, snapper turtles are not aggressive to humans and won’t actively attack humans unless threatened or provoked. Maybe it’ll turn out that after all, there was something much more dangerous lurking behind the seagrass than just a snapper turtle. 

Stern

Tortoisetrust

References

Br.de

National Geographic

Stern

Tortoise trust

Global warming makes apples taste sweeter

It turns out that there are more consequences to global warming than “just” a rise in global temperature – it can also affect the taste and texture of fruit and possibly vegetables.

Japanese researchers showed that the taste and texture of apples had changed as a result of global warming. Over the years, apples became sweeter but softer and more mealy, and less acid.

The scientists analysed data from apple cultivars “Fuji” und “Tsugaru”, which have been cultivated and harvested in the Nagano and Aomori Prefecture since the 1970s.

Over the course of 40 years, average temperature rose in both regions by 0.31 °C and 0.34 °C, and bud break and full bloom dates advanced, while culturing methods remained the same.

The “Fuji” apple is a world leading apple variety, and “Tsugaru” is the second most common variety in Japan. For Japan’s top two apple-producing regions, and probably many other regions that could be affected by a rise in temperature, climate change could have significant impact on agriculture.

References

"Changes in the taste and textural attributes of apples in response to climate change",Toshihiko Sugiura et al., 15 August 2013.
 

Rosalind E Franklin - The lady in the shadow of DNA

I was once asked to prepare a short presentation (for a job interview) about a scientist I found fascinating. As my title already indicates, I picked Rosalind Franklin. I think that talking about the life of a (famous) scientist is not only a good way to bring a personal aspect into science, but also a great way to learn more about the specific area and subject of the scientist.

Unfortunately, I didn’t get the job, but I really enjoyed preparing the presentation. I feel very passionate about this topic, so I thought I would put it to good use (or so I hope) and transform the information into a blog article.

Rosalind Elsie Franklin studied physical chemistry in Cambridge in the 1940s to become a biophysicist and x-ray crystallographer. In the early 20^th century (and to some extent still nowadays), it was rather unusually for women to a) work, and b) work in science, and c) be really successful in what they were doing (working in a field dominated by men).

After her studies (and during war time) she worked for the British Coal Utilisation Research Association. This work also formed the basis of her PhD, which she was awarded in 1945 by the University of Cambridge.

After several years of working in a French Research Institute, she came back to England (1951, Kings College, London), with a newly acquired research technique, x-ray crystallography. With this technique you can identify the location of atoms in a crystal, by looking at the image of the crystal under an x-ray beam.

In England, she joined Maurice Wilkins to work on DNA structure. By this time, DNA was known to be the only substance capable of storing all the information needed to create a living organism. What was not known was what the DNA molecule looked like or how it worked.

Her time in this lab was quite short, and it is said to have been one of her unhappiest times in her research career. So when she left in 1953 to start working with the tobacco mosaic virus (Birbeck University), focussing on her work about DNA was probably the last thing on her mind.

This might have been a big mistake, because it turned out, the work that she did on DNA, would one day make history.

In 1953, James Watson and Francis Crick published a (now really famous) paper in which they revealed that DNA was made up of a double helix. Yet, they did not do a single experiment for their research. In fact, their findings were based on a photograph, known as photograph 51, which Franklin took a year earlier with her assistant Raymond Gosling. And which Watson and Crick got hold off without her knowledge or permission.

Neither Rosalind, Wilkins nor Gosling were co-authors on that key paper, and her and Wilkins’ input was merely mentioned by Watson and Crick in an acknowledgement. Rosalind and Gosling, and Wilkins, did, however, publish two other papers, which appeared in the same nature issue.

With their publication, Watson and Crick had outrun everyone in the race to solving the mystery about the DNA structure—a race that nobody but (probably) Watson and Crick knew was a race. There is no evidence that Rosalind felt bitter about their achievement, nor that she knew that Watson’s and Crick’s conclusions and paper were based on her photo and the copy of a summary of her results she produced for a report.

Rosalind continued to work successfully at Birbeck University for the next 5 years until her death on April 16, 1958. She was only 37 when she died of ovarian cancer.

What I found so intriguing about her life is that she not only was a successful scientist who published almost 40 scientific papers in such a short career time, but that her “posthumous life” would reveal a lot of drama intrigues and scandals underneath the research on DNA. Because the story doesn’t end with her death, it probably only started with it!

Rosalind died without knowing what impact her photograph would have. In 1962, Watson, Crick and Wilkins received the Nobel Prize for their discovery of the double helix.

It still remains questionable if Rosalind would have been nominated, should she still have been alive.

The known tensions between her, Wilkins and Watson left (and still leave) a lot of room for speculation. Ever since, there was much debate about whether Watson and Crick would have been able to finish their hypothesis and model without Rosalind’s photograph (and ideas) and about whether Rosalind was wronged. But as it is, Nobel prizes cannot be awarded posthumously.

It is perhaps quite ironic (and/or rightful) that Rosalind really rose to popular fame and into the public eye in 1968, when Watson published his memoirs about the DNA discovery. The dismissive and belittling picture he painted about “Rosy” caused an outcry among women and scientist and catapulted Rosalind to fame.

In the same year (and following years), Rosalind's colleague from Birbeck, Aaron Klug, published several papers based on notes in Rosalind’s lab books that demonstrated how close she actually was to discovering the structure of DNA herself. So had she written in her lab books in early 1953, before the nature papers were published, that the “structure of the DNA had two chains”.

Rosalind Franklin could never witness the impact of her scientific contributions into the discovery of thedouble helix. But she was an impressive woman, who managed to succeed in academia in a time where not many women received recognition.  Her work at King’s was only a small part of her career. In her short life, she received international recognition for her important contributions in virology and carbonaceous solids, besides the study of DNA, and was no doubt respected by many scientists.

J.D Bernal once said about her: “As a scientist, Miss Franklin was distinguished by extreme clarity and perfection in everything she undertook. Her photographs are among the most beautiful x-ray photographs of any substance ever taken”.

Even Watson added the epilogue to a newer edition of the Double Helix:

“All of those people, should they so desire, can indicate events and details they remember differently. But there is one unfortunate exception. In 1958, Rosalind Franklin died at the early age of thirty-seven. Since my initial impressions of her, both scientific and personal (as recorded in the early pages of this book), were often wrong, I want to say something here about her achievements. The X-ray work she did at King's is increasingly regarded as superb. The sorting out of the A and B forms, by itself, would have made her reputation; even better was her 1952 demonstration using Patterson superposition methods, that the phosphate groups must be on the outside of the DNA molecule. Later, when she moved to Bernal's lab, she took up work on tobacco mosaic virus and quickly extended our qualitative ideas about helical construction into a precise quantitative picture, definitely establishing the essential helical parameters locating the ribonucleic chain halfway out from the central axis. Because I was then teaching in the States, I did not see her as often as did Francis (Crick), to whom she frequently came for advice or when she had done something very pretty, to be sure he agreed with her reasoning. By then, all traces of our early bickering were forgotten, and we both came to appreciate greatly her personal honesty and generosity, realising years too late the struggles that the intelligent woman faces to be accepted by a scientific world which often regards women as mere diversions from serious thinking. Rosalind's exemplary courage and integrity were apparent to all when, knowing she was mortally ill, she did not complain but continued working on a high level until a few weeks before her death.”

Further reads:

http://books.google.co.uk/books/about/Rosalind_Franklin.html?id=YbTh44KfkPIC&redir_esc=y

http://www.harpercollins.com/browseinside/index.aspx?isbn13=9780060985080

 

http://profiles.nlm.nih.gov/ps/retrieve/ResourceMetadata/KRBBJW

http://profiles.nlm.nih.gov/ps/retrieve/ResourceMetadata/KRBBHK

 

Crossfire of Sensations

Check out my article about synesthesia: Crossfire of sensations

I wish I were a synaesthesist. “A what?” you ask. No, I am not talking about a profession or a new religious cult. Synaesthesia is a “neurological condition”, although this description hardly does it justice. Imagine a world, where every word, letter, number, emotion or music comes with its own signature colour or taste. This is what it is like for a synaesthesist. Their world is colourful and tasteful because of a crossfire of senses. Synaesthesist can have blue Mondays, yellow Tuesdays, sour evenings or green threes, amongst others.

Synaesthesia comes from the ancient Greek words syn (union, together) and aisthēsis (sensation) meaning joined sensation. And that’s what it is—two independent senses experienced together1.

There are over 60 forms of synaesthesia2. In ‘grapheme-colour’ synaesthesia, words, letters and/or numbers are in colour and are often arranged in space. In ‘lexical-gustatory’ synaesthesia, words can elicit different tastes. Music or emotion can also evoke colours, and in the mirror-touch synaesthesia, people experience tactile sensations when they see others being touched. This is also associated with a heightened emphatic ability3. In a rarer form of synaesthesia, people see auras, coloured outlines, around other people and objects1.

Surprisingly, synaesthesia is relatively unknown and unresearched. The first documented case dates back to 18124, and synaesthesia has been more systematically described by Galton (1822-1911)5 later on, but after the early 1900s, research almost ceased.

Probably around 2-4% of the population have synaesthesia6. Many synaesthesists are not even aware that they experience the world differently to others, and sometimes only discover it by chance. Synaesthesia occurs from childhood on and people usually do not tend to lose it (and if they do lose it, usually it will be before the age of seven)1. Some forms of synaesthesia can be induced, either through accident, loss of a sense or drugs. In the early 1960s, it was shown that LSD can lead to synaesthesthetic experiences1,5. But it is unclear if the mechanisms are similar.

New research into synaesthesia has only recently been picked up again; but its mechanisms and causes remain partly unknown. Structural differences in the brain and/or interactions between different brain centres are thought to explain some of the mechanisms7,8. Cross wiring and cross activation between different regions in the brain could lead to different senses being experienced at the same time. But researchers are unsure if the cross wiring between different brain areas is caused by the connectivity between neurons or by chemicals1,5.

Brain imaging studies have also revealed differences in the brain anatomy. Synaesthesists appear to have connectivity clusters and the grey matter in some parts of the brain (parietal cortex and hippocampus) is thicker than in non-synaesthesists7,8. Researchers have also found increased connectivity and activity in centres processing texture, colour and form7,8, 13. Imaging techniques revealed that depending on the type of synaesthesia, centres processing taste, visual information or emotion are more active. Others suggest that the whole brain, and not just some areas, is strongly hyper-connected9.

Cases of synaesthesia are often common among family members, suggesting that a genetic component may be passed on through genes10. Although some similarities or patterns in the sensations can be observed between people, everyone experiences different sensations or combinations, even identical twins1. These combinations usually stay for life1.

Many synaesthesists work in the artistic industry. Some famous synaesthesists include the philosopher Ludwig Wittgenstein, the musician Miles Davis, the Nobel Prize physicist Richard Feynman, the author Vladimir Nabokov, and many more5.

I have to say that I envy synaesthesists a little bit. Although their sensations can lead to an overload of experiences at times, it must be amazing to see the world in technicolours. This “additional sense” shows us how fascinating the brain is and how little we still know about all its functions. Synaesthesia opens a new window of research for neuroscientists, philosophers and linguists, not only to understand this phenomenon, but also to learn more about brain mechanisms and individual differences in perception.

1.       Cytowic, R. E., & Eagleman, D. M. (2009). Wednesday is indigo blue: Discovering the brain of synesthesia. MIT Press.

2.    Spector, F., & Maurer, D. (2009). Synesthesia: a new approach to understanding the development of perception. Developmental psychology, 45(1), 175.

3.     Banissy, M. J., & Ward, J. (2007). Mirror-touch synesthesia is linked with empathy. Nature neuroscience, 10(7), 815-816.

4.     Jewanski, J., Day, S. A., & Ward, J. (2009). A colorful albino: the first documented case of synaesthesia, by Georg Tobias Ludwig Sachs in 1812. Journal of the History of the Neurosciences, 18(3), 293-303.

5.     Ward, J. (2013). Synesthesia. Annual Review of Psychology, 64, 49-75.

6.     Simner, J., Mulvenna, C., Sagiv, N., Tsakanikos, E., Witherby, S. A., Fraser, C. & Ward, J. (2006). Synaesthesia: The prevalence of atypical cross-modal experiences. Perception, 35(8), 1024.

7.     Rouw, R., & Scholte, H. S. (2007). Increased structural connectivity in grapheme-color synesthesia. Nature neuroscience, 10(6), 792-797.

8.     Rouw, R., Scholte, H. S., & Colizoli, O. (2011). Brain areas involved in synaesthesia: a review. Journal of Neuropsychology, 5(2), 214-242.

9.     Hänggi, J., Wotruba, D., & Jäncke, L. (2011). Globally altered structural brain network topology in grapheme-color synesthesia. The Journal of Neuroscience, 31(15), 5816-5828.

10.   Baron-Cohen, S., Burtlf, L., Smith-Laittan, F., Harrison, J., & Bolton, P. (1996). Synaesthesia: prevalence and familiality. Perception, 25, 1073-1079.