To Keep Pain In Check, Count Down

Kootenai Falls, Montana by Liang Ge

Henry Cabot Lodge Jr. presenting “The Thing” to the Security Council at the United Nations. 26 May 1960.

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“I want to empower women through dance. I think you can build confidence through movement. When a woman starts moving her body, and becomes comfortable with herself, and realizes that she can do the steps — it connects back to life. Because all of life is movement. Technically we’re dancing every day. And it doesn’t matter how you look. It matters how you move.”

NSF’s Science360 Photo of the Week

This is a close-up view of the beam created by a vortex laser.

Because the laser beam travels in a corkscrew pattern, encoding information into different vortex twists, it’s able to carry 10 times or more the amount of information than that of conventional lasers. The optics advancement could become a central component of next-generation computers designed to handle society’s growing demand for information sharing. Image credit: Natalia Litchinitser, University at Buffalo

Like this photo? Sign up for NSF’s Science360 News Service at news.science360.gov for a daily dose of STEM radio, news, videos and more cool images like this.

You can hold yourself back from the sufferings of the world, that is something you are free to do and it accords with your nature, but perhaps this very holding back is the one suffering you could avoid.

Franz Kafka (via man-of-prose)

How to Make a Motor Neuron

A team of scientists has uncovered details of the cellular mechanisms that control the direct programming of stem cells into motor neurons. The scientists analyzed changes that occur in the cells over the course of the reprogramming process. They discovered a dynamic, multi-step process in which multiple independent changes eventually converge to change the stem cells into motor neurons.

“There is a lot of interest in generating motor neurons to study basic developmental processes as well as human diseases like ALS and spinal muscular atrophy,” said Shaun Mahony, assistant professor of biochemistry and molecular biology at Penn State and one of the lead authors of the paper. “By detailing the mechanisms underlying the direct programing of motor neurons from stem cells, our study not only informs the study of motor neuron development and its associated diseases, but also informs our understanding of the direct programming process and may help with the development of techniques to generate other cell types.”

The direct programming technique could eventually be used to regenerate missing or damaged cells by converting other cell types into the missing one. The research findings, which appear online in the journal Cell Stem Cell on December 8, 2016, show the challenges facing current cell-replacement technology, but they also outline a potential pathway to the creation of more viable methods.

“Despite having a great therapeutic potential, direct programming is generally inefficient and doesn’t fully take into account molecular complexity,” said Esteban Mazzoni, an assistant professor in New York University’s Department of Biology and one of the lead authors of the study. “However, our findings point to possible new avenues for enhanced gene-therapy methods.”

The researchers had shown previously that they can transform mouse embryonic stem cells into motor neurons by expressing three transcription factors – genes that control the expression of other genes – in the stem cells. The transformation takes about two days. In order to better understand the cellular and genetic mechanisms responsible for the transformation, the researchers analyzed how the transcription factors bound to the genome, changes in gene expression, and modifications to chromatin at 6-hour intervals during the transformation.

“We have a very efficient system in which we can transform stem cells into motor neurons with something like a 90 to 95 percent success rate by adding the cocktail of transcription factors,” said Mahony. “Because of that efficiency, we were able to use our system to tease out the details of what actually happens in the cell during this transformation.”

“A cell in an embryo develops by passing through several intermediate stages,” noted Uwe Ohler, senior researcher at the Max Delbrück Center for Molecular Medicine (MDC) in Berlin and one of the lead authors of the work. “But in direct programming we don’t have that: we replace the gene transcription network of the cell with a completely new one at once, without the progression through intermediate stages. We asked, what are the timing and kinetics of chromatin changes and transcription events that directly lead to the final cell fate?“

The research team found surprising complexity – programming of these stem cells into neurons is the result of two independent transcriptional processes that eventually converge. Early on in the process, two of the transcription factors – Isl1 and Lhx3 – work in tandem, binding to the genome and beginning a cascade of events including changes to chromatin structure and gene expression in the cells. The third transcription factor, Ngn2, acts independently making additional changes to gene expression. Later in the transformation process, Isl1 and Lhx3 rely on changes in the cell initiated by Ngn2 to help complete the transformation. In order for direct programming to successfully achieve cellular conversion, it must coordinate the activity of the two processes.

“Many have found direct programming to be a potentially attractive method as it can be performed either in vitro – outside of a living organism – or in vivo – inside the body and, importantly, at the site of cellular damage,” said Mazzoni. “However, questions remain about its viability to repair cells – especially given the complex nature of the biological process. Looking ahead, we think it’s reasonable to use this newly gained knowledge to, for instance, manipulate cells in the spinal cord to replace the neurons required for voluntary movement that are destroyed by afflictions such as ALS.”

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."   

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.”