The promise of stem cells seems limitless. If they can be coaxed into rebuilding organs, repairing damaged spinal cords and restoring ravaged immune systems, these malleable cells would revolutionize medical treatment. But stem cell research is still in its infancy, as scientists seek to better understand the role of these cells in normal human development and disease.
On Friday, September 14, the Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research at Albert Einstein College of Medicine of Yeshiva University offered the Einstein community and invited guests an opportunity to hear from leading stem cell scientists investigating the dynamic field. The 2012 Einstein Stem Cell Institute Symposium featured speakers from around the globe presenting the latest research on induced pluripotent stem cells (iPS cells), cell reprogramming, as well as cancer and hematopoietic (blood-forming) stem cells.
"This symposium was an important milestone for stem cell research at Einstein and confirms our intent to contribute to advances in stem cell biology," said the event’s host and organizer, Paul Frenette, M.D., director and chair of Einstein’s Stem Cell Institute and professor of medicine and of cell biology.
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Kangaroo Mother Care - a technique in which a breastfed premature infant remains in skin-to-skin contact with the parent’s chest rather than being placed in an incubator - has lasting positive impact on brain development, revealed Universite Laval researchers in the October issue of Acta Paediatrica. Very premature infants who benefited from this technique had better brain functioning in adolescence - comparable to that of adolescents born at term - than did premature infants placed in incubators.
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A University of Arizona professor is overseeing the manufacture of an experimental drug that could help reduce brain damage after a stroke.
The drug, known as 3K3A-APC, currently is undergoing clinical trials in Europe to determine its safety in humans after proving effective in animal models at reducing brain damage and improving motor skills after a stroke when given in combination with another commonly used stroke therapy.
Thomas Davis, professor of pharmacology in the UA College of Medicine, was chosen to direct the manufacture of the drug for human trials after co-authoring a recent paper in the journal Stroke that pointed to the drug’s effectiveness in rats and mice when used in conjunction with a clot-busting therapy known as tissue plasminogen activator, or tPA.
While tPA is commonly given to sufferers of ischemic stroke, which results from an obstruction in a blood vessel supplying blood to the brain, the therapy poses significant challenges when administered alone, including a limited treatment window, Davis said.
"It has to be given within the first three to four and a half hours of the stroke," Davis said. "It only works in 10 percent of the patients, and it causes bleeding, so tPA alone isn’t that effective."
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Neurodegenerative diseases such as Alzheimer’s or Parkinson’s are characterised by the loss of nerve cells and the deposition of proteins in the brain tissue. A group of researchers led by Gabor G. Kovacs from the Clinical Institute of Neurology at the MedUni Vienna has now demonstrated that Alzheimer’s disease does not just – as previously believed – involve the proteins that are attributed to Alzheimer’s, but instead the condition can involve a mixture of interacting proteins from different neurodegenerative diseases.
“As a result, Alzheimer’s should not be treated in isolation. According to these latest findings, pure, classical Alzheimer’s disease, which involves only the attributed proteins tau and amyloid beta, appears not to be the norm,” says Kovacs. There is also a varied regional distribution of nerve cell loss and protein deposits between patients which, taken together, have clinical prognostic significance. As a consequence of this, differentiated strategies need to be developed for personalised therapy that takes account of all the interacting factors.
The new treatment concepts which are currently being developed by the MedUni Vienna’s neuropathologists, neurobiologists, neurologists, psychiatrists and neuroimaging experts will divide the patients into “sub-groups”. Says Kovacs: “The aim is to define these groups very precisely in future in order to be able to offer them personalised treatment.”
Dementia diseases: a growing trend
Around 100,000 Austrians are currently suffering from a dementia-related illness, according to statistics from the Austrian Alzheimer Society. According to estimates, this figure will rise to around 280,000 by 2050 as a result of the increasing age of the general population. Alzheimer’s disease is responsible for 60 to 80 per cent of these conditions.
The global Alzheimer’s report by “Alzheimer’s Disease International” reckons that the prevalence of dementia doubles every 20 years. There are currently around 35 million people worldwide suffering a dementia-related illness. By 2030, their number will rise to 65.7 million and reach as many as 115.4 million by 2050.
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UK scientists have made a breakthrough in a new method of brain tumor diagnosis, offering hope to tens of thousands of people.
Researchers, led by Professor Francis Martin of Lancaster Environment Centre at Lancaster University, have shown that infrared and Raman spectroscopy – coupled with statistical analysis – can be used to tell the difference between normal brain tissue and the different tumor types that may arise in this tissue, based on its individual biochemical-cell ‘fingerprint’.
Spectroscopy is a technique that allows us to analyse light interactions with samples such as tissue by generating a spectrum, which is a reflection of the interrogated sample.
Currently, when surgeons are operating to remove a brain tumor it can be difficult to spot where the tumor ends and normal tissue begins.
But new research published online in Analytical Methods this month has shown it is possible to spot the difference between diseased and normal tissue using Raman spectroscopy – a type of spectroscopy which works effectively on living tissue, giving accurate results in seconds.
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At this year’s Tokyo Games Show, Japanese purveyor of electronically-augmented fashion Neurowear unveiled the successor to its Necomimi brain-activated cat ears. It’s called Shippo, and it’s a brain-controlled motorized tail that responds to the user’s current emotional state with corresponding wagging.
Shippo requires a NeuroSky electroencephalograph (EEG) headset, alongside a clip-on heart monitor, in order to observe brain activity and pick up on the user’s emotional state. This information is then translated to wagging, which will be soft and slow or hard and fast, depending on whether one is relaxing or excited/anxious. The EEG headset communicates with the fluffy appendage via a Bluetooth connection.
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Duchess the elephant has UK’s first cataract op
Zookeepers are carefully monitoring an elephant who was the first in the UK to undergo an eye operation, to discover how much of her sight has returned.
Duchess was said to be recovering well after yesterday’s operation to remove a cataract from her left eye.
Paignton Zoo’s 42-year-old African elephant had her right eye removed in 2011 because of glaucoma, and has lately become practically blind.
Neil Bemment, curator of mammals and director of operations at the zoo, said staff had high hopes for the operation’s success. “It couldn’t have gone better,” he said. “She went down very smoothly under the anaesthetic and the operation went as well as we could hope.”
Mr Bemment said Duchess was still “disorientated” from the procedure and was being kept out of view with plenty of reassurance from staff.
"Her sight had deteriorated to the point where she could only tell the difference between light and shade," Mr Bemment said. "We’re hoping that his will restore her sight for most distances. She won’t be able to read about herself in the newspaper, but we’re hopeful that she will be more familiar in her surroundings."
(Source: thisisdevon.co.uk)
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The real culprits of colour blindness are vision cells rather than unusual wiring in the eye and brain, recent research has shown.
The discovery brings scientists a step closer to restoring full colour vision for people who are colour blind – a condition that affects close to two million Australians, says Professor Paul Martin from The Vision Centre and The University of Sydney.
It may also help pave the way for an answer to one of the most common causes of blindness – age-related macular degeneration (AMD), which accounts for half of the legal blindness cases in Australia.
“There are millions of cones in our eyes – vision cells that pick up bright light and allow us to see colour,” Prof. Martin says. “They are nicknamed red, green and blue cones because they are sensitive to different wavelengths of light.
“We now know that in the macular region of the eye, each cone has its own ’private line’ into the optic nerve and the brain. Just as a painter can mix from three tubes of paint to produce a wide and vivid palette, our brain uses the ‘private lines’ from the three cone types to create thousands of colour sensations.
Scientists previously thought that full colour vision depends on specialised nerve wiring in the eye and brain, but animal studies show that the wiring is identical for monkeys whether they have normal or abnormal colour vision, Prof. Martin says.
“This tells us that there’s nothing wrong in the brain – it’s only working with the signals that it receives on the ‘private lines’,” he says. “So the only difference in normal and abnormal colour vision is caused by the first stage of sight, which points to faulty cones. Either they have failed to develop, or else they are picking up abnormal wavelengths.
“Now that we know faulty wiring isn’t the cause, we can concentrate on fixing the cones, which are controlled by genes – and thus prone to mutation or mistakes during cell replication. There are already promising results from gene therapy as a way to restore full colour vision in colour blind monkeys.”
“While we have still have some way to go, the benefits of this gene therapy – if successful – can potentially extend beyond providing complete colour vision,” he says.
“If we can get these genes to work in human eyes, it means that the same approach might be possible for other visual problems – including blinding diseases such as macular degeneration.”
"In macular degeneration, energy supplies to the macula can’t keep up with demand. So the ‘private line’ system must be very energy-intensive. Gene therapy could be used to turn down the cones’ energy demand, or to increase energy supply from supporting cells to cone cells,” Prof. Martin says.
“Together with clinical researchers at the Save Sight Institute, we are now working hard to find out exactly how many ‘private lines’ there are in humans. That can point us to where energy demand is highest and we can target gene therapy to the right place.
"So animal research on ‘private lines’ for colour vision has given new clues for understanding one of the most important visual diseases – macular degeneration – in humans."
(Source: scinews.com.au)
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Researchers at Cold Spring Harbor Laboratory (CSHL) have solved an important piece of one of neuroscience’s outstanding puzzles: how progenitor cells in the developing mammalian brain reproduce themselves while also giving birth to neurons that will populate the emerging cerebral cortex, the seat of cognition and executive function in the mature brain.
CSHL Professor Linda Van Aelst, Ph.D., and colleagues set out to solve a particular mystery concerning radial glial cells, or RGCs, which are progenitors of pyramidal neurons, the most common type of excitatory nerve cell in the mature mammalian cortex.
In genetically manipulated mice, Van Aelst’s team demonstrated that a protein called DOCK7 plays a central regulatory role in the process that determines how and when an RGC “decides” either to proliferate, i.e., make more progenitor cells like itself, or give rise to cells that will mature, or “differentiate,” into pyramidal neurons. The findings are reported in the September 2012 issue of Nature Neuroscience
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At any given moment, millions of cells are on the move in the human body, typically on their way to aid in immune response, make repairs, or provide some other benefit to the structures around them. When the migration process goes wrong, however, the results can include tumor formation and metastatic cancer. Little has been known about how cell migration actually works, but now, with the help of some tiny worms, researchers at the California Institute of Technology (Caltech) have gained new insight into this highly complex task.
The team’s findings are outlined this week online in the early edition of the Proceedings of the National Academy of Sciences (PNAS).
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