Cambridge University

Anti-ageing chocolate which reduces wrinkles developed by Cambridge University spin-off

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A daily 7.5g bar of the chocolate can change the underlying skin stucture of a 50 year old to that of someone in their 30s, say developers

It may seem too good to be true, but guilt-free chocolate which promises to slow down the emergence of wrinkles and sagging skin, has been developed by scientists.

‘Esthechoc’ the brainchild of a Cambridge University spin-off lab, claims to boost antioxidant levels and increase circulation to prevent lines and keep skin looking youthful and smooth.

Just a small 7.5g bar of anti-ageing chocolate contains the same amount of the antioxidant astaxanthin as a fillet of Alaskan salmon, and equal levels of free-radical fighting cocoa polyphenols as 100g of dark chocolate.

Its makers say it can change the underlying skin of a 50-60 year old into that of someone in their 20s or 30s. Tests showed that after four weeks of eating the anti-ageing chocolate every day, volunteers had less evidence of inflammation in their blood and increased blood supply to skin tissue.

Creator Dr Ivan Petyaev, a former researcher at Cambridge University, and founder of biotech firm Lycotec, said: “We’re using the same antioxidant that keeps goldfish gold and flamingos pink.

“In clinical trials we saw that inflammation in the skin starting to go down and the tissues began to benefit.

“We used people in their 50s and 60s and in terms of skin biomarkers we found it had brought skin back to the levels of a 20 or 30 year old. So we’ve improved the skin’s physiology.

“People using it claimed that their skin was better and we can see that the product is working to slow down ageing.”

As the bar contains just 38kcal its makers say it is even safe for diabetics.

But ‘Esthechoc’ is unlikely to be available in Britain’s corner shops. The confectionary, which is also called ‘Cambridge Beauty Chocolate’ comes boxed as a three week supply, individually wrapped, and will only be available in high end retailers from next month.

It is also likely to come with a hefty price tag, although it’s makers were unwilling to reveal the cost before its official launch at the Global Food Innovation Summit in London next month.

How the chocolate will look

According to its brochure the target market are ‘elegant, educated and affluent’ city-dwelling women in their 30s, and businessmen ‘to support their appearance in a stressful environment and on their business travels.’

However health experts were cautious about the product,

Naveed Sattar, Professor of Metabolic Medicine at Glasgow University, said more robust clinical trials would be needed to validate the ‘ridiculously strong’ claims made by the company.

“There may be biological reasons to think some of the compounds may benefit some processes linked to ageing and disease but on the other hand, eating too much chocolate means more calories, which means obesity so the net effect is never clear cut.

“These food claims need to be back up with trials to have any genuine credibility. Such trials are glaring by their absence so all such health claims are unfounded.”

Nutrition experts at University College London also warned that previous trials showed that astaxanthin worked better when applied directly to the face rather than ingested.

UCL nutritionist Dr George Grimble said: “There is a potentially sound scientific base to this although it is obviously early days.

“There needs to be further clinical trials to show that it is safe but astaxanthin has been shown to have antioxidant effects and low toxicity, so from that respect, it seems promising.

“Using dark chocolate is quite clever. As a nutritionist, I am generally in favour of dark chocolate.

“So it’s got a good track record in terms of the science but it is too early to say what the long term benefits might be.

“In my humble opinion, it would be necessary for the company’s in-house trial to be submitted for publication in a peer-reviewed journal in order for their health claims to be substantiated.”

Scientists ‘print’ new eye cells

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human eye
Many teams are researching different ways to repair the sight-giving cells of the retina

Scientists say they have been able to successfully print new eye cells that could be used to treat sight loss.

The proof-of-principle work in the journal Biofabrication was carried out using animal cells.

The Cambridge University team says it paves the way for grow-your-own therapies for people with damage to the light-sensitive layer of tissue at back of the eye – the retina.

More tests are needed before human trials can begin.

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This is a step in the right direction as the retina is often affected in many of the common eye conditions, causing loss of central vision which stops people watching TV and seeing the faces of loved ones”

Clara Eaglen of the RNIB

At the moment the results are preliminary and show that an inkjet printer can be used to print two types of cells from the retina of adult rats―ganglion cells and glial cells.

These are the cells that transmit information from the eye to certain parts of the brain, and provide support and protection for neurons.

The printed cells remained healthy and retained their ability to survive and grow in culture.

Retinal repair

Co-authors of the study Prof Keith Martin and Dr Barbara Lorber, from the John van Geest Centre for Brain Repair at the University of Cambridge, said: “The loss of nerve cells in the retina is a feature of many blinding eye diseases. The retina is an exquisitely organised structure where the precise arrangement of cells in relation to one another is critical for effective visual function.

Human eye
The retina sits at the back of the eye

“Our study has shown, for the first time, that cells derived from the mature central nervous system, the eye, can be printed using a piezoelectric inkjet printer. Although our results are preliminary and much more work is still required, the aim is to develop this technology for use in retinal repair in the future.”

They now plan to attempt to print other types of retinal cells, including the light-sensitive photoreceptors – rods and cones.

Scientists have already been able to reverse blindness in mice using stem cell transplants.

And there is promising work into electronic retina implants implants in patients.

Clara Eaglen, of the RNIB, said: “Clearly it’s still at a very early stage and further research is needed to develop this technology for use in repairing the retina in humans.

“The key to this research, once the technology has moved on, will be how much useful vision is restored.

“Even a small bit of sight can make a real difference, for some people it could be the difference between leaving the house on their own or not.

“It could help boost people’s confidence and in turn their independence.”

Prof Jim Bainbridge of London’s Moorfields Eye Hospital said: “The finding that eye cells can survive the printing process suggests the exciting possibility that this technique could be used in the future to create organised tissues for regeneration of the eye and restoration of sight.

“Blindness is commonly caused by degeneration of nerve cells in the eye. In recent years there has been substantial progress towards the development of new treatments involving cell transplantation.”

Stem cell transplant repairs damaged gut in mouse model of inflammatory bowel disease.

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A source of gut stem cells that can repair a type of inflammatory bowel disease when transplanted into mice has been identified by researchers at the Wellcome Trust–Medical Research Council Cambridge Stem Cell Institute at the University of Cambridge and at BRIC, the University of Copenhagen, Denmark.

The findings pave the way for patient-specific regenerative therapies for inflammatory bowel diseases such as ulcerative colitis.

All tissues in our body contain specialised stem cells, which are responsible for the lifelong maintenance of the individual tissue and organ. Stem cells found in adults are restricted to their tissue of origin, for example, stem cells found in the  will be able to contribute to the replenishment of the gut whereas stem cells in the skin will only contribute to maintenance of the skin.

The team first looked at developing intestinal tissue in a mouse embryo and found a population of stem cells that were quite different to the  that have been described in the gut. The cells were very actively dividing and could be grown in the laboratory over a long period without becoming specialised into the adult counterpart. Under the correct growth conditions, however, the team could induce the cells to form mature intestinal tissue.

When the team transplanted these cells into mice with a form of , within three hours the stem cells had attached to the damaged areas of the mouse intestine and integrated with the gut cells, contributing to the repair of the damaged tissue.

Dr Kim Jensen, a Wellcome Trust researcher and Lundbeckfoundation fellow, who led the study, said: “We found that the cells formed a living plaster over the damaged gut. They seemed to respond to the environment they had been placed in and matured accordingly to repair the damage.

“One of the risks of  like this is that the cells will continue to expand and form a tumour, but we didn’t see any evidence of that with this immature stem cell population from the gut.”

Cells with similar characteristics were isolated from both mice and humans and the team were also able to generate similar cells by reprogramming adult human cells, so called induced Pluripotent Stem Cells (iPSCs), and growing them in the appropriate conditions.

“We’ve identified a source of gut  that can be easily expanded in the laboratory, which could have huge implications for treating human inflammatory bowel diseases. The next step will be to see whether the human cells behave in the same way in the mouse transplant system and then we can consider investigating their use in patients,” added Dr Jensen.

Study shows side-channel phone risk via microphone and camera.

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Researchers exploring smartphone security vulnerabilities are increasingly turning to information about smartphone sensors as pathways to security breach. Earlier this year, a Stanford University team warned that sensors such as accelerometers could identify a device and track it. In 2012, a paper titled “Practicality of Accelerometer Side Channels on Smartphones” by researchers from the University of Pennsylvania reported that by analyzing data gathered by accelerometers they were able to get a good idea of the PIN or pattern used to protect a phone. Now a study by two researchers at Cambridge University set out to show that a smartphone PIN can be identified via the smartphone camera and microphone. Smartphone rsearchers Ross Anderson, Professor of Security Engineering at the Computer Laboratory at the University of Cambridge and Laurent Simon, also of the Computer Laboratory, demonstrated an attack that can reveal the PIN codes for sensitive apps, such as those for banking, by tapping into the microphone and camera.. They wrote about their finding in the paper, “PIN Skimmer: Inferring PINs Through the Camera and Microphone.” Their study was presented at a recent workshop on Security and Privacy in Smartphones and Mobile Devices (SPSM) in Berlin.

“In this paper,” they wrote, “we aim to raise awareness of side-channel attacks even when strong isolation protects sensitive applications. Previous works have studied the use of the phone accelerometer and gyroscope as side channel data to infer PINs. Here, we describe a new side-channel attack that makes use of the video and to infer PINs entered on a number-only soft key-board on a smartphone.”

Their attack was achieved through a program called PIN Skimmer. They found that codes entered on a number-only soft keypad could be identified. Their feat involves software that watches the smartphone user’s face by means of the camera and listens to clicks through the microphone as the victim types. The microphone can detect touch as a user enters the PIN, taking in the clicks made by the smartphone from the user pressing on the virtual number keys. The camera estimates the orientation of the phone as the user is doing this and correlates it to the position of the user-tapped digit.

Writing about their work in the security weblog “Light Blue Touchpaper,” Ross Anderson said, “We found that software on your can work out what PIN you’re entering by watching your face through the camera and listening for the clicks as you type. Previous researchers had shown how to work out PINs using the gyro and accelerometer; we found that the camera works about as well. We watch how your face appears to move as you jiggle your phone by typing.”

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The paper reported these results: When selecting from a test set of 50 four-digit PINs, PIN Skimmer correctly infers more than 30 percent of PINs after two attempts, and more than 50 percent of PINs after five attempts on Android-powered phones. When selecting from a set of 200 eight-digit PINs, PIN Skimmer correctly infers about 45 percent of the PINs after five attempts and 60 percent after 10 attempts.

The authors reserved a special section in the paper where they presented possible countermeasures to mitigate side-channel attacks on PIN input. Blogged Anderson: “Meanwhile, if you’re developing payment apps, you’d better be aware that these risks exist.”

Metabolism ‘obesity excuse’ true

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Obese child

The mocked “obesity excuse” of being born with a slow metabolism is actually true for some people, say researchers.

A team at the University of Cambridge has found the first proof that mutated DNA does indeed slow metabolism.

The researchers say fewer than one in 100 people are affected and are often severely obese by early childhood.

The findings, published in the journal Cell, may lead to new obesity treatments even for people without the mutation.

Scientists at the Institute of Metabolic Science, in Cambridge, knew that mice born without a section of DNA, a gene called KSR2, gained weight more easily.

It slows the ability to burn calories and that’s important as it’s a new explanation for obesity”

Prof Sadaf Farooqi University of Cambridge

But they did not know what affect it may be having in people, so they analysed the DNA of 2,101 severely obese patients.

Some had mutated versions of KSR2.

It had a twin effect of increasing their appetite while their slowing metabolism.

“You would be hungry and wanting to eat a lot, you would not want to move because of a slower metabolism and would probably also develop type 2 diabetes at a young age,” lead researcher Prof Sadaf Farooqi told the BBC.

She added: “It slows the ability to burn calories and that’s important as it’s a new explanation for obesity.”

Munching on chips
The mutation delivers a double-whammy by increasing the drive to eat and reducing calorie burn

KSR2 is mostly active in the brain and it affects the way individual cells interpret signals, such as the hormone insulin, from the blood. This in turn affects the body’s ability to burn calories.

Prof Farooqi said the metabolism argument had been derided by doctors, as well as wider society, due to a lack of evidence that metabolism was slowed in obese patients. In many cases obese patients have an elevated metabolism to cope with fuelling a much larger body.

She said less than 1% of people had mutated versions of the gene and some would be a normal weight, but about 2% of children who were obese by the age of five would have the mutated gene.

However, if drugs could be developed to target problems with KSR2, then it might be beneficial to anyone who is too fat.

“Other genetic disorders, such as in blood pressure, have shown that even where there’s a normal gene, targeting the pathway can still help,” Prof Farooqi said.

The amount and types of food eaten, as well as levels of exercise, directly affect weight, but some people at more risk of becoming obese that others.

Obesity can run in families. The other obesity genes that have been discovered tend to affect appetite.

People have two copies of the FTO gene – one from each parent – and each copy comes in a high- and a low-risk form. Those with two-high risk copies of the FTO gene are thought to be 70% more likely to become obese than those with low-risk genes.

It makes fatty foods more tempting and alters levels of the hunger hormone ghrelin.

Dr Katarina Kos, from the University of Exeter Medical School, said: “It is an exciting and interesting breakthrough, this is a new pathway predisposing people to obesity.

“But it does exist in obese and lean people so you still need the obesogenic environment.”

Secret of Usain Bolt’s speed unveiled.

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Scientists say they can explain Usain Bolt‘s extraordinary speed with a mathematical model.

His 100m time of 9.58 seconds during the 2009 World Championships in Berlin is the current world record.

They say their model explains the power and energy he had to expend to overcome drag caused by air resistance, made stronger by his frame of 6ft 5in.

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Writing in the European Journal of Physics, the team hope to discover what makes extraordinary athletes so fast.

According to the mathematical model proposed, Bolt’s time of 9.58 seconds in Berlin was achieved by reaching a speed of 12.2 metres per second, equivalent to about 27mph.

Less dynamic

The team calculated that Bolt’s maximum power occurred when he was less than one second into the race and was only at half his maximum speed. This demonstrates the near immediate effect of drag, which is where air resistance slows moving objects.

They also discovered less than 8% of the energy his muscles produced was used for motion, with the rest absorbed by drag.

When comparing Bolt’s body mass, the altitude of the track and the air temperature, they found out that his drag coefficient – which is a measure of the drag per unit area of mass – was actually less aerodynamic than that of the average man.

Effects of drag

Jorge Hernandez of the the National Autonomous University of Mexico said: “Our calculated drag coefficient highlights the outstanding ability of Bolt. He has been able to break several records despite not being as aerodynamic as a human can be.

“The enormous amount of work that Bolt developed in 2009, and the amount that was absorbed by drag, is truly extraordinary.

“It is so hard to break records nowadays, even by hundredths of a second, as the runners must act very powerfully against a tremendous force which increases massively with each bit of additional speed they are able to develop.

“This is all because of the ‘physical barrier’ imposed by the conditions on Earth. Of course, if Bolt were to run on a planet with a much less dense atmosphere, he could achieve records of fantastic proportions.

“The accurate recording of Bolt’s position and speed during the race provided a splendid opportunity for us to study the effects of drag on a sprinter.

bolt

“If more data become available in the future, it would be interesting to see what distinguishes one athlete from another,” added Mr Hernandez.

Bolt’s time in Berlin was the biggest increase in the record since electronic timing was introduced in 1968.

Large stride

John Barrow at Cambridge University who has previously analysed how Bolt could become even faster, explained that his speed came in part due his “extraordinary large stride length”, despite having such an initial slow reaction time to the starting gun.

“He has lots of fast twitch muscle fibres that can respond quickly, coupled with his fast stride is what gives him such an extraordinary fast time.”

He said Bolt has lots of scope to break his record if he responded faster at the start, ran with a slightly stronger tail-wind and at a higher altitude, where there was less drag.

Bolt’s Berlin record was won with a tail wind of only 0.9m per second, which didn’t give him “the advantage of helpful wind assistance”, he added.

“You’re allowed to have a wind no greater than 2m per second to count for record purposes, so without becoming any faster he has huge scope to improve,” Prof Barrow told BBC News.

Source: BBC