Spinal Stimulators Repurposed To Restore Touch In Lost Limb

In California’s Salinas Valley, known as the “Salad Bowl of the World,” a push is underway to expand agriculture’s adoption of technology. Special correspondent Cat Wise reports on how such innovation is providing new opportunities for the Valley’s largely Hispanic population. Watch her full piece here: http://to.pbs.org/2gLmEga

Self-assembling nanoparticle arrays can switch between a mirror and a window

By finely tuning the distance between nanoparticles in a single layer, researchers have made a filter that can change between a mirror and a window.

The development could help scientists create special materials whose optical properties can be changed in real time. These materials could then be used for applications from tuneable optical filters to miniature chemical sensors.

Creating a ‘tuneable’ material - one which can be accurately controlled - has been a challenge because of the tiny scales involved. In order to tune the optical properties of a single layer of nanoparticles - which are only tens of nanometres in size each - the space between them needs to be set precisely and uniformly.

To form the layer, the team of researchers from Imperial College London created conditions for gold nanoparticles to localise at the interface between two liquids that do not mix. By applying a small voltage across the interface, the team have been able to demonstrate a tuneable nanoparticle layer that can be dense or sparse, allowing for switching between a reflective mirror and a transparent surface. The research is published today in Nature Materials.

Read more.

Directly Reprogramming a Cell's Identity with Gene Editing

Researchers have used CRISPR—a revolutionary new genetic engineering technique—to convert cells isolated from mouse connective tissue directly into neuronal cells.

In 2006, Shinya Yamanaka, a professor at the Institute for Frontier Medical Sciences at Kyoto University at the time, discovered how to revert adult connective tissue cells, called fibroblasts, back into immature stem cells that could differentiate into any cell type. These so-called induced pluripotent stem cells won Yamanaka the Nobel Prize in medicine just six years later for their promise in research and medicine.

Since then, researchers have discovered other ways to convert cells between different types. This is mostly done by introducing many extra copies of “master switch” genes that produce proteins that turn on entire genetic networks responsible for producing a particular cell type.

Now, researchers at Duke University have developed a strategy that avoids the need for the extra gene copies. Instead, a modification of the CRISPR genetic engineering technique is used to directly turn on the natural copies already present in the genome.

These early results indicate that the newly converted neuronal cells show a more complete and persistent conversion than the method where new genes are permanently added to the genome. These cells could be used for modeling neurological disorders, discovering new therapeutics, developing personalized medicines and, perhaps in the future, implementing cell therapy.

The study was published on August 11, 2016, in the journal Cell Stem Cell.

“This technique has many applications for science and medicine. For example, we might have a general idea of how most people’s neurons will respond to a drug, but we don’t know how your particular neurons with your particular genetics will respond,” said Charles Gersbach, the Rooney Family Associate Professor of Biomedical Engineering and director for the Center for Biomolecular and Tissue Engineering at Duke. “Taking biopsies of your brain to test your neurons is not an option. But if we could take a skin cell from your arm, turn it into a neuron, and then treat it with various drug combinations, we could determine an optimal personalized therapy.”

“The challenge is efficiently generating neurons that are stable and have a genetic programming that looks like your real neurons,” says Joshua Black, the graduate student in Gersbach’s lab who led the work. “That has been a major obstacle in this area.”

In the 1950s, Professor Conrad Waddington, a British developmental biologist who laid the foundations for developmental biology, suggested that immature stem cells differentiating into specific types of adult cells can be thought of as rolling down the side of a ridged mountain into one of many valleys. With each path a cell takes down a particular slope, its options for its final destination become more limited.

If you want to change that destination, one option is to push the cell vertically back up the mountain—that’s the idea behind reprogramming cells to be induced pluripotent stem cells. Another option is to push it horizontally up and over a hill and directly into another valley.

“If you have the ability to specifically turn on all the neuron genes, maybe you don’t have to go back up the hill,” said Gersbach.

Previous methods have accomplished this by introducing viruses that inject extra copies of genes to produce a large number of proteins called master transcription factors. Unique to each cell type, these proteins bind to thousands of places in the genome, turning on that cell type’s particular gene network. This method, however, has some drawbacks.

“Rather than using a virus to permanently introduce new copies of existing genes, it would be desirable to provide a temporary signal that changes the cell type in a stable way,” said Black. “However, doing so in an efficient manner might require making very specific changes to the genetic program of the cell.”

In the new study, Black, Gersbach, and colleagues used CRISPR to precisely activate the three genes that naturally produce the master transcription factors that control the neuronal gene network, rather than having a virus introduce extra copies of those genes.

CRISPR is a modified version of a bacterial defense system that targets and slices apart the DNA of familiar invading viruses. In this case, however, the system has been tweaked so that no slicing is involved. Instead, the machinery that identifies specific stretches of DNA has been left intact, and it has been hitched to a gene activator.

The CRISPR system was administered to mouse fibroblasts in the laboratory. The tests showed that, once activated by CRISPR, the three neuronal master transcription factor genes robustly activated neuronal genes. This caused the fibroblasts to conduct electrical signals—a hallmark of neuronal cells. And even after the CRISPR activators went away, the cells retained their neuronal properties.

“When blasting cells with master transcription factors made by viruses, it’s possible to make cells that behave like neurons,” said Gersbach. “But if they truly have become autonomously functioning neurons, then they shouldn’t require the continuous presence of that external stimulus.”

The experiments showed that the new CRISPR technique produced neuronal cells with an epigenetic program at the target genes matching the neuronal markings naturally found in mouse brain tissue.

“The method that introduces extra genetic copies with the virus produces a lot of the transcription factors, but very little is being made from the native copies of these genes,” explained Black. “In contrast, the CRISPR approach isn’t making as many transcription factors overall, but they’re all being produced from the normal chromosomal position, which is a powerful difference since they are stably activated. We’re flipping the epigenetic switch to convert cell types rather than driving them to do so synthetically.”

The next steps, according to Black, are to extend the method to human cells, raise the efficiency of the technique and try to clear other epigenetic hurdles so that it could be applied to model particular diseases.

“In the future, you can imagine making neurons and implanting them in the brain to treat Parkinson’s disease or other neurodegenerative conditions,” said Gersbach. “But even if we don’t get that far, you can do a lot with these in the lab to help develop better therapies.”

You are the center of wonderland & Keep the last glow in mind by Jana Luo

New discovery could be a major advance for understanding neurological diseases

The discovery of a new mechanism that controls the way nerve cells in the brain communicate with each other to regulate our learning and long-term memory could have major benefits to understanding how the brain works and what goes wrong in neurodegenerative disorders such as epilepsy and dementia. The breakthrough, published in Nature Neuroscience, was made by scientists at the University of Bristol and the University of Central Lancashire.   The findings will have far-reaching implications in many aspects of neuroscience and understanding how the brain works.

The human brain contains around 100-billion nerve cells, each of which makes about 10,000 connections to other cells, called synapses. Synapses are constantly transmitting information to, and receiving information from other nerve cells. A process, called long-term potentiation (LTP), increases the strength of information flow across synapses. Lots of synapses communicating between different nerve cells form networks and LTP intensifies the connectivity of the cells in the network to make information transfer more efficient. This LTP mechanism is how the brain operates at the cellular level to allow us to learn and remember. However, when these processes go wrong they can lead to neurological and neurodegenerative disorders.

Precisely how LTP is initiated is a major question in neuroscience. Traditional LTP is regulated by the activation of special proteins at synapses called NMDA receptors. This study, by Professor Jeremy Henley and co-workers reports a new type of LTP that is controlled by kainate receptors.

This is an important advance as it highlights the flexibility in the way synapses are controlled and nerve cells communicate. This, in turn, raises the possibility of targeting this new pathway to develop therapeutic strategies for diseases like dementia, in which there is too little synaptic transmission and LTP, and epilepsy where there is too much inappropriate synaptic transmission and LTP.

Jeremy Henley, Professor of Molecular Neuroscience in the University’s School of Biochemistry in the Faculty of Biomedical Sciences, said: “These discoveries represent a significant advance and will have far-reaching implications for the understanding of memory, cognition, developmental plasticity and neuronal network formation and stabilisation. In summary, we believe that this is a groundbreaking study that opens new lines of inquiry which will increase understanding of the molecular details of synaptic function in health and disease.”

Dr Milos Petrovic, co-author of the study and Reader in Neuroscience at the University of Central Lancashire added: “Untangling the interactions between the signal receptors in the brain not only tells us more about the inner workings of a healthy brain, but also provides a practical insight into what happens when we form new memories. If we can preserve these signals it may help protect against brain diseases.

“This is certainly an extremely exciting discovery and something that could potentially impact the global population. We have discovered potential new drug targets that could help to cure the devastating consequences of dementias, such as Alzheimer’s disease. Collaborating with researchers across the world in order to identify new ways to fight disease like this is what world-class scientific research is all about, and we look forward to continuing our work in this area.”

Earlier this year, The Lutetium Project explored how microfluidic circuits are made, and now they are back with the conclusion of their microfluidic adventures. This video explores how microfluidic chips are used and how microscale fluid dynamics relates to other topics in the field. Because these techniques allow researchers very fine control over droplets, there are many chemical and biological possibilities for microfluidic experiments, some of which are shown in the video. Microfluidics in medicine are also already more common than you may think. For example, test strips used by diabetic patients to measure their blood glucose levels are microfluidic circuits! (Video and image credit: The Lutetium Project; submitted by Guillaume D.)

Shortly after he finished filming on the opulent set of Baz Luhrmann’s ‘The Great Gatsby,’ Joel headed off to the Jordanian desert to begin training for 'Zero Dark Thirty.'  With a heavy dose of mock horror, he said that it was quite a shock to his delicate system:

“An experience like ‘Gatsby’ really spoils you because you are treated like a king. You’re given a big trailer, someone brings fresh flowers to your trailer, there are dates and walnuts and coconut water in your fridge … really living large.“

Then, when he suddenly found himself roughing it in the torrid desert, “sharing a cubicle with five other guys, half of them military, and carrying 50-60 kilos of equipment … It was like, 'Baz!  Come and save me!’  You get a reality check."