TYPE 1 DIABETES ? A CURE IS HIGHLY POSSIBLE 

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Laboratory mouse (stock image). In this study, researchers found that two nuclear receptors play critical roles in the development of TH17 cells, and that by targeting these receptors, they were able to stop autoimmunity from developing in several mouse models, sparing beta cells.

Credit: © mrks_v / Fotolia

In new research published in Endocrinology, Thomas Burris, Ph.D., chair of pharmacological and physiological science at Saint Louis University, reports that his team has found a way to prevent type I diabetes in an animal model.

Type I diabetes is a chronic autoimmune disease that occurs when the body's immune system destroys insulin producing pancreatic beta cells, resulting in insulin deficiency and hyperglycemia. Current treatments for type I diabetes focus on controlling blood sugar with insulin therapy and must continue throughout a person's life.

Burris and his research team focused on blocking the autoimmune process that destroys beta cells and leads to diabetes, with the aim of developing therapies that can prevent the illness from developing rather than treating its symptoms.

"None of the animals on the treatment developed diabetes even when we started treatment after significant beta cell damage had already occurred. We believe this type of treatment would slow the progression of type I diabetes in people or potentially even eliminate the need for insulin therapy," said Burris.

Scientists already knew that at least two types of immune "T-cells" contribute to the development of type I diabetes. However, the role of a third type, TH17, remained unclear.

In this study, researchers found that two nuclear receptors play critical roles in the development of TH17 cells, and that by targeting these receptors, they were able to stop autoimmunity from developing in several mouse models, sparing beta cells.

The team blocked the receptors (ROR alpha and gamma t) with SR1001 (a selective ROR alpha and gamma t inverse agonist developed by Burris), significantly reducing diabetes in mice that were treated with it.

These results confirm that TH17 cells likely play a key role in the development of type I diabetes and suggest that the use of drugs that target this cell type may offer a new treatment for the illness.

Scientists develop protein with potential to modify brain function, memory in mice and fish

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Scientists at USC have developed a new tool to modify brain activity and memory in targeted ways, without the help of any drugs or chemicals. (Stock image)

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Scientists at USC have developed a new tool to modify brain activity and memory in targeted ways, without the help of any drugs or chemicals.

The GFE3 protein may help researchers map the brain's connections and better understand how inhibitory synapses modulate brain function, said lead author Don B. Arnold, a professor of biological sciences at USC Dornsife College of Letters, Arts and Sciences.

It also may enable them to control neural activity and lead to advancements in research for diseases or conditions ranging from schizophrenia to cocaine addiction, Arnold said.

The new tool is a protein that carries a death sentence for synaptic proteins in specific cells. The protein can be encoded in animal genomes to effectively switch off their inhibitory synapses -- connections between neurons -- increasing their electrical activity.

"GFE3 harnesses a little known and remarkable property of proteins within the brain," Arnold said.

The protein takes advantage of an intrinsic process -- the brain's cycle of degrading and replacing proteins. Most brain proteins last only a couple of days before they are actively degraded and replaced by new proteins. GFE3 targets proteins that hold inhibitory synapses together to this degradation system and as a result, the synapses fall apart.

"Rather than a cell deciding when a protein needs to be degraded, we sort of hijack the process," Arnold said.

For the study published in the journal Nature Methods on June 6, the team of scientists studied the protein's effect in both mice and zebrafish. The researchers found that GFE3 protein triggered the neurons on the two sides of the spine to work in opposition, generating uncoordinated movements.

Previously, drugs could be used to inhibit inhibitory synapses in the brain, for instance benzodiazapines, which treat anxiety, insomnia or seizures. But the drugs inhibit all the cells in a particular area, not just the neurons that are the intended target.

"Unfortunately, cells that have very different, even opposite functions tend to be right next to each other in the brain," Arnold said. "Thus, pharmacological experiments are especially difficult to interpret. By encoding GFE3 within the genome, we can target and modulate the inhibitory synapses of specific cells without affecting other cells that have different functions."

Bionic leaf turns sunlight into liquid fuel

New system surpasses efficiency of photosynthesis

The days of drilling into the ground in the search for fuel may be numbered,because if Daniel Nocera has his way, it'll just be a matter of looking for sunny skies.

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A new "bionic leaf" system uses solar energy to produce liquid fuel.

Nocera, the Patterson Rockwood Professor of Energy at Harvard University, and Pamela Silver, the Elliott T. and Onie H. Adams Professor of Biochemistry and Systems Biology at Harvard Medical School, have co-created a system that uses solar energy to split water molecules and hydrogen-eating bacteria to produce liquid fuels.

The paper, whose lead authors include post-doctoral fellow Chong Liu and graduate student Brendan Colón, is described in a June 3 paper published in Science.

"This is a true artificial photosynthesis system," Nocera said. "Before, people were using artificial photosynthesis for water-splitting, but this is a true A-to-Z system, and we've gone well over the efficiency of photosynthesis in nature."

While the study shows the system can be used to generate usable fuels, its potential doesn't end there, said Silver, who is also a Founding Core Member of the Wyss Institute at Harvard University.

"The beauty of biology is it's the world's greatest chemist -- biology can do chemistry we can't do easily," she said. "In principle, we have a platform that can make any downstream carbon-based molecule. So this has the potential to be incredibly versatile."

Dubbed "bionic leaf 2.0," the new system builds on previous work by Nocera, Silver and others, which -- though it was capable of using solar energy to make isopropanol -- faced a number of challenges.

Chief among those challenges, Nocera said, was the fact that the catalyst used to produce hydrogen -- a nickel-molybdenum-zinc alloy -- also created reactive oxygen species, molecules that attacked and destroyed the bacteria's DNA. To avoid that problem, researchers were forced to run the system at abnormally high voltages, resulting in reduced efficiency.

"For this paper, we designed a new cobalt-phosphorus alloy catalyst, which we showed does not make reactive oxygen species," Nocera said. "That allowed us to lower the voltage, and that led to a dramatic increase in efficiency."

The system can now convert solar energy to biomass with 10 percent efficiency, Nocera said, far above the one percent seen in the fastest growing plants.

In addition to increasing the efficiency, Nocera and colleagues were able to expand the portfolio of the system to include isobutanol and isopentanol. Researchers also used the system to create PHB, a bio-plastic precursor, a process first demonstrated by MIT professor Anthony Sinskey.

The new catalyst also came with another advantage -- its chemical design allows it to "self-heal" -- meaning it wouldn't leech material into solution.

"This is the genius of Dan," Silver said. "These catalysts are totally biologically compatible."

Though there may yet be room for additional increases in efficiency, Nocera said the system is already effective enough to consider possible commercial applications but within a different model for technology translation.

"It's an important discovery--it says we can do better than photosynthesis," Nocera said. "But I also want to bring this technology to the developing world as well."

Working in conjunction with the First 100 Watts program at Harvard, which helped fund the research, Nocera hopes to continue developing the technology and its applications in nations like India with the help of their scientists.

In many ways, Nocera said, the new system marks the fulfillment of the promise of his "artificial leaf" -- which used solar power to split water and make hydrogen fuel.

"If you think about it, photosynthesis is amazing," he said. "It takes sunlight, water and air--and then look at a tree. That's exactly what we did, but we do it significantly better, because we turn all that energy into a fuel."

DO YOU WANT TO REGAIN YOUR YOUTH?

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Jennifer Lemon, Research Associate, Department of Biology, McMaster University.

Credit: McMaster University

A dietary supplement containing a blend of thirty vitamins and minerals -- all natural ingredients widely available in health food stores -- has shown remarkable anti-aging properties that can prevent and even reverse massive brain cell loss, according to new research from McMaster University.

It's a mixture scientists believe could someday slow the progress of catastrophic neurological diseases such as Alzheimer's, ALS and Parkinson's.

"The findings are dramatic," says Jennifer Lemon, research associate in the Department of Biology and a lead author of the study. "Our hope is that this supplement could offset some very serious illnesses and ultimately improve quality of life."

The formula, which contains common ingredients such as vitamins B, C and D, folic acid, green tea extract, cod liver oil and other nutraceuticals, was first designed by scientists in McMaster's Department of Biology in 2000.

A series of studies published over the last decade and a half have shown its benefits in mice, in both normal mice and those specifically bred for such research because they age rapidly, experiencing dramatic declines in cognitive and motor function in a matter of months.

The mice used in this study had widespread loss of more than half of their brain cells, severely impacting multiple regions of the brain by one year of age, the human equivalent of severe Alzheimer's disease.

The mice were fed the supplement on small pieces of bagel each day over the course of several months. Over time, researchers found that it completely eliminated the severe brain cell loss and abolished cognitive decline.

"The research suggests that there is tremendous potential with this supplement to help people who are suffering from some catastrophic neurological diseases," says Lemon, who conducted the work with co-author Vadim Aksenov, a post-doctoral fellow in the Department of Biology at McMaster.

"We know this because mice experience the same basic cell mechanisms that contribute to neurodegeneration that humans do. All species, in fact. There is a commonality among us all."

In addition to looking at the major markers of aging, they also discovered that the mice on the supplements experienced enhancement in vision and most remarkably in the sense of smell -- the loss of which is often associated with neurological disease -- improved balance and motor activity.

The next step in the research is to test the supplement on humans, likely within the next two years, and target those who are dealing with neurodegenerative diseases. The research is published online in the journal Environmental and Molecular Mutagenesis.

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Story Source:

The above post is reprinted from materials provided by McMaster University. Note: Materials may be edited for content and length.

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Journal Reference:

1. J.A. Lemon, V. Aksenov, R. Samigullina, S. Aksenov, W.H. Rodgers, C.D. Rollo, D.R. Boreham. A multi-ingredient dietary supplement abolishes large-scale brain cell loss, improves sensory function, and prevents neuronal atrophy in aging mice. Environmental and Molecular Mutagenesis, 2016; DOI: 10.1002/em.22019

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McMaster University. "Fountain of youth? Dietary supplement may prevent and reverse severe damage to aging brain, research suggests." ScienceDaily. ScienceDaily, 2 June 2016. <www.sciencedaily.com/releases/2016/06/160602095204.htm>.

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