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Tuesday, March 5, 2013

Vitamin C essential for muscles



The University of Otago   

 
newart-graphics_Muscle_shutterstock
Muscle is the largest store of vitamin C in our bodies, and is sensitive to the intake dropping below the equivalent of two kiwifruits a day.
Image: newart-graphics/Shutterstock
A daily vitamin C intake equivalent to eating two kiwifruit a day is required to ensure our muscles maintain optimal levels, researchers from the University of Otago, Christchurch have found.
Professor Margreet Vissers and her team from the Centre for Free Radical Research are involved in a large on-going study to better understand the critical role of vitamin C in the human body. They are also investigating the best way to obtain the vitamin from the diet.
Their paper on the uptake of vitamin C into muscle has just been published in the American Journal of Clinical Nutrition, the most prestigious publication in the field of nutrition science.
The study has shown that skeletal muscle is very sensitive to changes in vitamin C intake and that the vitamin C content in muscle will fall if intake decreases below optimal levels. This is likely to affect muscle function. Muscle is the largest store of vitamin C in our bodies.
Professor Vissers and her team gave 54 males aged between 18 and 35 either half a kiwifruit or two kiwifruit a day over a six week period. They then measured the vitamin C content in muscle and elsewhere in the body.
The researchers found that general energy levels were increased with the ‘two per day’ kiwifruit dose, and this is likely to reflect the optimal muscle function under these conditions.
She says eating high-value vitamin C foods, like kiwifruit, is the ideal way to maintain healthy levels.
 “Many people think that all fruit and vegetables are equally able to supply vitamin C, but this is not the case. The levels in food vary hugely across the spectrum. We should eat a good range daily, but because many fruit contain only one tenth of a healthy daily vitamin C requirement, we would recommend at least one serve per day of a high-value food like kiwifruit. This will help you easily reach an optimal vitamin C intake, as well as delivering other vital nutrients.’’
The study was funded by Zespri International and the University of Otago.
Editor's Note: Original news release can be found here.

Greens crucial for immune cells



Walter and Eliza Hall Institute   
 
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The new study shows how crucial eating green leafy vegetables can be for protecting the body.
Image: Elena Elisseeva/Shutterstock
Eating your greens may be even more important that previously thought, with the discovery that an immune cell population essential for intestinal health could be controlled by leafy greens in your diet.
The immune cells, named innate lymphoid cells (ILCs), are found in the lining of the digestive system and protect the body from ‘bad’ bacteria in the intestine. They are also believed to play an important role in controlling food allergies, inflammatory diseases and obesity, and may even prevent the development of bowel cancers.
Dr Gabrielle Belz, Ms Lucie Rankin, Dr Joanna Groom and colleagues from the Walter and Eliza Hall Institute’s Molecular Immunology division have discovered the gene T-bet is essential for producing a population of these critical immune cells and that the gene responds to signals in the food we eat.
Dr Belz said the research team revealed T-bet was essential for generating a subset of ILCs which is a newly discovered cell type that protects the body against infections entering through the digestive system. “In this study, we discovered that T-bet is the key gene that instructs precursor cells to develop into ILCs, which it does in response to signals in the food we eat and to bacteria in the gut,” Dr Belz said. “ILCs are essential for immune surveillance of the digestive system and this is the first time that we have identified a gene responsible for the production of ILCs.”
The research was published today in the journal Nature Immunology.
Dr Belz said that the proteins in green leafy (cruciferous) vegetables are known to interact with a cell surface receptor that switches on T-bet, and might play a role in producing these critical immune cells. “Proteins in these leafy greens could be part of the same signalling pathway that is used by T-bet to produce ILCs,” Dr Belz said. “We are very interested in looking at how the products of these vegetables are able to talk to T-bet to make ILCs, which will give us more insight into how the food we eat influences our immune system and gut bacteria.”
ILCs are essential for maintaining the delicate balance between tolerance, immunity and inflammation. Ms Rankin said the discovery had given the research team further insight into external factors responsible for ILC activation. “Until recently, it has been difficult to isolate or produce ILCs,” Ms Rankin said. “So we are very excited about the prospect for future research on these cells which are still poorly understood.”
ILCs produce a hormone called interleukin-22 (IL-22), which can protect the body from invading bacteria, Dr Belz said. “Our research shows that, without the gene T-bet, the body is more susceptible to bacterial infections that enter through the digestive system. This suggests that boosting ILCs in the gut may aid in the treatment of these bacterial infections,” she said.
ILCs help to maintain a ‘healthy’ environment in the intestine by promoting good bacteria and healing small wounds and abrasions that are common in the tissues of the gut. They may also have a role in resolving cancerous lesions. “The discovery of these immune cells has thrown open a completely new way of looking at gut biology,” Dr Belz said. “We are just starting to understand how important these immune cells are in regulating allergy and inflammation, and the implications for bowel cancer and other gastrointestinal disorders such as Crohn’s disease,” she said.
“Understanding the biology of ILCs and the genes that are essential for generating them will help us to develop methods of targeting these cells,” Dr Belz said. “This might include boosting ILCs in situations where they may not be active enough, such as infections or some cancers, or depleting them in situations where they are overactive, such as chronic inflammatory disease,” she said.
This project was supported by the National Health and Medical Research Council of Australia, the Sylvia and Charles Viertel Foundation, the Howard Hughes Medical Institute and the Victorian Government.
Editor's Note: Original news release can be found here.

Wednesday, February 27, 2013

Language, uniquely, makes us human



Amy Marshall, Centenary Institute   
 
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FOXP2 is our 'language gene' and has a unique sequence in humans.
Image:Shutterstock
We humans tend to consider ourselves apart from other species. But we’re not really so different. So what makes us unique? I’d say it’s language, though not everyone would agree.
Some people insist it’s our large brains, but dolphins have proportionally larger brains than we do. Some still contend our opposable thumbs set us apart, but koalas have two thumbs on each hand.
We walk on two legs? Yes, of course, but the feathered species do that too.
Some are insistent that our individuality as a species rests on the fact we can use tools, but many diverse vertebrate species are tool-users, including primates, elephants and birds. Even the veined octopus and certain ants and wasps have been observed using tools.
The answer, then, is… language. We uniquely have the ability to communicate complex and abstract ideas.
At first it was spoken language. Then, independently, several human cultures developed the written word – the means to communicate with others over thousands of miles or years.
Through language we have built civilisations, developed science and medicine, literature and philosophy. We do not have to learn everything from personal experience, because through language we can learn from the experience of others.
Language makes us human, and it’s encoded in our DNA.
The language gene
FOXP2, known as the “language gene”, has a unique sequence in humans. While other living mammals share identical amino acids at two key amino positions 303 and 325, these amino acids are different in humans (threonine to asparagine at amino acid 303 and asparagine to serine at amino acid 325).
Such substitution mutations occurred some time after we diverged from our common ancestor with the chimpanzee 4-8 million years ago.
We shared this unique FOXP2 protein sequence with both Neanderthals and Denisovans, from which we diverged somewhere in the region of 400,000 years ago.
Compared to these other hominids, humans have an additional mutation in a region that regulates FOXP2 gene expression. Was it this latest mutation in FOXP2 that ensured our survival through better communication, as other hominids went extinct?
This mutation was swiftly incorporated into the human genome at high frequencies during the last 50,000 years suggesting it carries a survival advantage. Studies to understand the effect of this most recent change in FOXP2 are currently underway.
The FOXP2 gene is involved in brain development, particularly those areas involved in vocal behaviour. FOXP2 is particularly important for animals, including songbirds such as finches, canaries and parrots that learn to sing by imitation.
In the songbird brain, FOXP2 expression is highest when birds are learning to sing. Reduction of FOXP2 expression in the brain of zebra finches at this critical period left birds unable to completely or accurately learn to sing.
In humans, FOXP2 mutations are associated with severe speech and language deficits known as developmental verbal dyspraxia – affecting both the ability to coordinate vocal muscles in speech and causing language comprehension difficulties. What a terrible, isolating condition that must be.
In language we find both truth and beauty; then, being human, we use it to argue about what is true and beautiful.
Language is fundamentally what makes us what we are. Would you disagree? If so, please, use your voice and let me know.
Editor's Note: This article was originally published by The Conversation, here, and is licenced as Public Domain under Creative Commons. See Creative Commons - Attribution Licence.