#Key component for terahertz wireless networks Terahertz radiation could one day provide the backbone for wireless systems that can deliver data up to one hundred times faster than today's cellular or Wi-fi networks.
But there remain many technical challenges to be solved before terahertz wireless is ready for prime time.
Researchers from Brown University have taken a major step toward addressing one of those challenges. They've developed
Multiplexers are devices that enable separate streams of data to travel through a single medium.
It's the technology that makes it possible for a single cable to carry multiple TV channels
or for a fiber optic line to carry thousands of phone calls at the same time.""Any terahertz communications application is going to need some form of multiplexing
professor of engineering at Brown and senior author of a paper describing the new device."
Today's cellular and Wi-fi networks rely on microwaves to carry voice conversations and data. But the increasing demands for data transfer are quickly becoming more than microwaves can handle.
Terahertz waves have a much higher frequency and therefore more potential bandwidth. Scientists and engineers have begun only recently exploring the potential of terahertz waves, however.
As a result, many of the components for a terahertz wireless network--including multiplexers--have not yet been developed.
The multiplexer that Mittleman and his colleagues have been working on makes use of what's known as a leaky wave antenna.
In this case the antenna is made from two metal plates placed in parallel to form a waveguide.
One of the plates has a small slit in it. As terahertz waves travel down the waveguide, some of the radiation leaks out of the slit.
It turns out that terahertz waves leak out a different angles depending on their frequency.""That means if you put in 10 different frequencies between the plates--each of them potentially carrying a unique data stream--they'll come out at 10 different angles,
"Mittleman said.""Now you've separated them and that's demultiplexing.""On the other end, a receiver could be tuned to accept radiation at a particular angle,
thus receiving data from only one stream.""We think it's definitely a reasonable solution to meet the needs of a terahertz communication network,
"said Nicholas Karl, a graduate student at Brown and the paper's lead author. Karl led the experiments on the device with fellow graduate student Robert Mckinney.
Other authors on the study are Rajind Mendis, a research professor at Brown, and Yasuaki Monnai from Keio University in Tokyo.
One of the advantages to the approach, the researchers say, is that by adjusting the distance between the plates,
it's possible to adjust the spectrum bandwidth that can be allocated to each channel. That could be especially useful
when such a device is deployed for use in a data network.""For example, if one user suddenly needs a ton of bandwidth,
you can take it from others on the network who don't need as much just by changing the plate spacing at the right location,
"Mittleman said. The group plans to continue its work to refine the device. A research group from Osaka University is collaborating with Mittleman's group to implement the device in a prototype terahertz network they're building."
"This is a first-generation, proof-of-concept device, "Karl said.""There are still things we can do to improve it
and we'll continue to study it.""Mittleman hopes that the work will challenge other researchers to start developing components for terahertz networks."
"The biggest impact this may have is it may just be the kick that people need to start thinking about this issue,
"Mittleman said.""That means they'll start coming up with clever ideas that are entirely different from this one
#Lung'filtering'technique can reduce transplant rejection University of Manchester researchers have used a new technique to recondition poorly functioning lungs
and remove donor white blood cells in an attempt to increase the number of lungs available for transplant,
and at the same time reduce the risk of acute rejection. Lung transplantation is often the only option for patients with end stage lung disease,
but is limited by a shortage of donor organs. When waiting list patients are lucky enough to receive a transplant,
they need lifelong immunosuppression to prevent their own immune system from destroying the transplanted organ, a process called acute rejection.
The University researchers, in collaboration with a team from the University of Lund in Sweden, used a new technique called ex-vivo lung perfusion (EVLP) where the lung is kept alive, breathing outside the body and supported by a supply
This can repair an organ that would normally be turned down for transplant. Given that 80%of donor lungs are used currently not
Dr James Fildes, from the University's Collaborative Centre for Inflammation Research and the Transplant Centre at the University Hospital of South Manchester NHS Foundation Trust, led the study.
"Because the lung is a potential entry route for infection into the body, its immune response is developed highly.
"All of this makes lung transplant recipients particularly susceptible to rejection, so they require continuous immunosuppression,
which then increases the risk of infection and cancer. These immune processes are therefore very important and contribute to the outlook where only five out of ten patients will survive for at least five years."
"The Manchester and Sweden team took lungs from pigs and transplanted them either using the normal transplant method or after three hours of EVLP,
and the recipients were monitored for 24 hours. In the EVLP lungs there was little evidence of rejection, whereas in the normal transplant method, all the lungs showed signs of severe rejection.
EVLP is becoming an established technique, but this is the first time it has been used in this way. The researchers are hopeful that EVLP will be used in patients to reduce high rates of rejection and wastage of scarce donor lungs.
As the lungs were monitored only for 24 hours it is difficult to know the long-term effects but even a delay would be beneficial in allowing the transplanted organ to become accepted.
"EVLP opens up new possibilities in one of the most problematic areas of surgery.""Patricia Moore, 63, from Oswestry was diagnosed with idiopathic pulmonary fibrosis in 2011 and received a transplant in 2014.
She said:""The side-effects of immunosuppression are potentially unpleasant and the thought of the associated bronchoscopy terrifies me.
the work showcases the new technology and its practical importance in clinical science by showing how it has given new insights into Alzheimer's disease plaques."
and collected data that may resolve several current issues regarding the pathology of Alzheimer's disease. While Superman's x-ray vision is only the stuff of comics, our method,
By combining Scales with Abscale--a variation for immunolabeling--and Chemscale--a variation for fluorescent chemical compounds--they generated multicolor high-resolution 3d images of amyloid beta plaques in older mice from a genetic mouse
model of Alzheimer's disease developed at the RIKEN BSI by Takaomi Saido team. After showing how Scales treatment can preserve tissue
the researchers put the technique to practical use by visualizing in 3d the mysterious"diffuse"plaques seen in the postmortem brains of Alzheimer's disease patients that are typically undetectable using 2d imaging.
but not in later stages of the disease after the plaques have accumulated.""Clearing tissue with Scales followed by 3d microscopy has clear advantages over 2d stereology or immunohistochemistry,"states Miyawaki."
not only for visualizing plaques in Alzheimer's disease, but also for examining normal neural circuits and pinpointing structural changes that characterize other brain diseases
#Biodiesel made easier, cleaner with waste-recycling catalyst Researchers at Cardiff University have devised a way of increasing the yield of biodiesel by using the waste left over from its production process.
Using simple catalysis, the researchers have been able to recycle a non-desired by-product produced when biodiesel is formed from vegetable oil,
Fuel suppliers are required also to reduce the greenhouse gas intensity of the EU fuel mix by 6 per cent by 2020 in comparison to 2010.
The work is currently in its early stages and in future studies the researchers will look to optimise the design of the catalyst
Lead author of the study Professor Graham Hutchings, Director of the Cardiff Catalysis Institute, said:"
"Co-author of the study Professor Stuart Taylor, Deputy Director of the Cardiff Catalysis Institute, said:"
which waste is dealt with, and seriously improve the quality of life by reducing carbon emissions from fossil fuels and encourage efficient use of resources."
"Professor Matthew Rosseinsky, Professor of Inorganic chemistry at the University of Liverpool, who was not part of the study,
said:""This paper shows how fundamental catalysis research can develop new mild processes to enhance the sustainability of biodiesel.
As well as offering new opportunities for industry, it will stimulate the search for even better basic catalysts
#New leukemia gene stops blood cells'growing up'Scientists have identified a gene--FOXC1--that, if switched on, causes more aggressive cancer in a fifth of acute myeloid leukemia (AML) patients,
according to a Cancer Research UK study published in the journal Cancer cell, today. The FOXC1 gene is switched normally on during embryonic development
and is needed to turn cells into specialised tissues, like the eyes, kidney, brain and bone.
But this new research found that in certain patients with AML--a type of blood cancer that affects white blood cells
and the bone marrow--this gene was switched wrongly on inside the patient's cancer cells. When it is switched on in blood cell tissue
This triggers the cancer to be more aggressive, as young cells are able to replicate more than mature cells--causing cancer cells to grow faster
Of these, around 20 per cent would have had the FOXC1 gene wrongly switched on in their cancer.
Dr Tim Somervaille, lead author from the Cancer Research UK Manchester Institute at The University of Manchester,
which makes the cancer grow more rapidly.""There are certain situations where this gene is necessary,
it causes more aggressive forms of leukemia.""Nell Barrie, senior science communication manager at Cancer Research UK, said:"
"It's essential that we continue to research basic biology to further understand how cells become cancerous.
In this study, identifying a specific gene behind more aggressive forms of acute myeloid leukemia could give clues for new ways to personalise treatments for select patients.
The better we understand the nuts and bolts of each cancer, the sooner we can find new ways to stop it
#Microbiologists describe new insights into human neurodegenerative disease Microbiology researchers at the University of Georgia studying a soil bacterium have identified a potential mechanism for neurodegenerative diseases.
A role for the protein HSD10 had been suspected in patients with Alzheimer's disease and Parkinson's disease, but no direct connection had previously been established.
This new breakthrough suggests that HSD10 reduces oxidative stress, promotes cell repair and prevents cellular death.
The authors first discovered that an enzyme related to HSD10, Csga, produces energy during sporulation in the bacterium Myxococcus xanthus.
Csga was found to degrade the phospholipid cardiolipin into fragments that were used as energy sources during sporulation much the same way humans produce
and protects the energy-making machinery from oxidative stress. HSD10 is a versatile protein with many known functions
but its role in oxidative stress has remained a mystery. The authors showed that HSD10 preferentially degrades highly toxic cardiolipin peroxides
free radical produced during oxidative stress that would normally initiate apoptosis, or cell death. HSD10 activity is inhibited strongly
when bound to the amyloid beta peptide so prevalent in Alzheimer's disease.""Normally, apoptosis is beneficial for regulating multicellular systems,
"said the study's lead author Tye Boynton, a postdoctoral research associate in the Franklin College of Arts and Sciences."
"But with rampant oxidative stress leading to uncontrolled cellular death, you end up with diseases such as Alzheimer's and Parkinson's.
HSD10 potentially prevents this by removing these damaged lipids before they have a chance to act."
"When cardiolipin becomes damaged by oxidative stress, the newly formed cardiolipin peroxides induce apoptosis instead of energy production.
The UGA research team, led by microbiology professor Lawrence Shimkets, showed for the first time that HSD10 can mitigate oxidative damage."
"This research suggests that HSD10 prevents neurodegeneration by destroying cardiolipin peroxides and provides a fresh perspective on the etiology of Alzheimer's disease that could inform novel drug strategies,
"Shimkets said d
#Filling a void in stem cell therapy Stem cell therapies are limited often by low survival of transplanted stem cells
and the lack of precise control over their differentiation into the terminal cell types needed to repair
or replace injured tissues. Now, a team led by Wyss Institute Core Faculty member David Mooney, Ph d.,has developed a new strategy--embedding stem cells into porous,
transplantable hydrogels--that has improved experimentally bone repair by boosting the survival rate of transplanted stem cells
and influencing their cell differentiation. Mooney--who is also the Robert P. Pinkas Family Professor of Bioengineering at the Harvard John A. Paulson School of engineering
and Applied sciences (SEAS)--and his team published their findings in the September 14 issue of Nature Materials.
The team included Georg Duda, Ph d.,who a Wyss Associate Faculty member and the director of the Julius Wolff Institute and Professor of Biomechanics and Musculoskeletal Regeneration at Charité--Universitätsmedizin Berlin,
and Wyss Institute Founding Director Donald Ingber, M d.,Ph d.,who is also the Judah Folkman Professor of Vascular Biology at Harvard Medical school and Boston Children's Hospital and Professor of Bioengineering
AT SEAS. Stem cell therapies bear tremendous hopes for the repair of many tissues and bone or even the replacement of entire organs.
Tissue-specific stem cells can now be generated in the laboratory. However no matter how well they grow in the laboratory,
and function correctly at the site of injury to be useful for clinical regenerative therapies.
To improve the therapeutic ability of transplanted stem cells, Mooney's team has drawn inspiration from naturally occurring stem cell"niches."
a Graduate student who worked with Mooney and who is the study's first author.""Based on our experience with mechanosensitive stem cells, we hypothesized that hydrogels could be leveraged to generate the right chemical and mechanical cues in a first model of bone regeneration."
By coupling the bulk gel with a small peptide derived from the extracellular environment of genuine stem cell niches,
"The collaborative, cross-disciplinary work was supported by the Harvard university Materials Research Science and Engineering Center (MRSEC),
#Building the electron superhighway TV screens that roll up. Roofing tiles that double as solar panels. Sun powered cell phone chargers woven into the fabric of backpacks.
A new generation of organic semiconductors may allow these kinds of flexible electronics to be manufactured at low cost,
says University of Vermont physicist and materials scientist Madalina Furis. But the basic science of how to get electrons to move quickly
and easily in these organic materials remains murky. To help, Furis and a team of UVM materials scientists have invented a new way to create
what they are calling"an electron superhighway"in one of these materials--a low-cost blue dye called phthalocyanine--that promises to allow electrons to flow faster and farther in organic semiconductors Their discovery,
reported Sept. 14 in the journal Nature Communications, will aid in the hunt for alternatives to traditional silicon-based electronics.
Hills and Potholes Many of these types of flexible electronic devices will rely on thin films of organic materials that catch sunlight
and convert the light into electric current using excited states in the material called"excitons.""Roughly speaking, an exciton is displaced a electron bound together with the hole it left behind.
Increasing the distance these excitons can diffuse--before they reach a juncture where they're broken apart to produce electrical current--is essential to improving the efficiency of organic semiconductors.
Using a new imaging technique, the UVM team was able to observe nanoscale defects and boundaries in the crystal grains in the thin films of phthalocyanine--roadblocks in the electron highway."
"We have discovered that we have hills that electrons have to go over and potholes that they need to avoid,
and photoluminescence to optically probe the molecular structure of the phthalocyanine crystals.""Marrying these two techniques together is new;
"says Lane Manning'08 a doctoral student in Furis'lab and co-author on the new study.
and the boundaries in the crystals influence the movement of excitons. It's these boundaries that form a"barrier for exciton diffusion,
And then, with this enhanced view,"this energy barrier can be eliminated entirely, "the team writes.
the team worked in the lab of UVM physics and materials science professor Randy Headrick to successfully form films with jumbo-sized crystal grains and"small angle boundaries."
Better Solar cells Though the Nature Communications study focused on just one organic material, phthalocyanine, the new research provides a powerful way to explore many other types of organic materials, too--with particular promise for improved solar cells.
A recent U s. Department of energy report identified one of the fundamental bottlenecks to improved solar power technologies as"determining the mechanisms by
which the absorbed energy (exciton) migrates through the system prior to splitting into charges that are converted to electricity."
"The new UVM study--led by two of Furis'students, Zhenwen Pan G'12, and Naveen Rawat G'15--opens a window to view how increasing"long-range order"in the organic semiconductor films is a key mechanism that allows excitons to migrate farther."
"The molecules are stacked like dishes in a dish rack, "Furis explains, "these stacked molecules--this dish rack--is the electron superhighway."
--and can't be pushed by voltage like the electrons flowing in a light bulb--they can, in a sense, bounce from one of these tightly stacked molecules to the next.
This allows organic thin films to carry energy along this molecular highway with relative ease,
"One of today's big challenges is how to make better photovoltaics and solar technologies,"says Furis,
who directs UVM's program in materials science, "and to do that we need a deeper understanding of exciton diffusion.
That's what this research is about
#Loss of cellular energy leads to neuronal dysfunction in neurodegenerative disease model A new study from the Gladstone Institutes shows for the first time that impairments in mitochondria--the brain's cellular power plants--can deplete cellular energy levels
and cause neuronal dysfunction in a model of neurodegenerative disease. A link between mitochondria, energy failure,
and neurodegeneration has long been hypothesized. However, no previous studies were able to comprehensively investigate the connection because sufficiently sensitive tests,
or assays, were not available to measure ATP (the energy unit of the cell that is generated by mitochondria) in individual neurons.
In the current study which was chosen as the Paper of the Week in the Journal of Biological Chemistry,
the scientists created novel assays to more accurately measure the brain's energy production. Using a model of Leigh's disease,
a genetically inherited neurodegenerative disorder that affects mitochondria, the researchers tested energy levels in neurons using the new assays.
They found that the genetic mutation associated with Leigh's disease compromised ATP levels, and this reduction of ATP was enough to cause significant cellular dysfunction."
"It was assumed always that defects in mitochondria would result in a depletion of energy levels,
which would be toxic to neurons, "says first author Divya Pathak, Phd, a postdoctoral fellow in the Gladstone Institute of Neurological disease."
"But no one had been able to prove this because the necessary assays were not available. Now that we've demonstrated the link between impaired mitochondria, a loss of ATP,
and neuronal dysfunction, the next step is to see if this connection holds true in conditions like Parkinson's disease and Alzheimer's disease."
"Applying their new assay in healthy neurons, the researchers also determined the energy threshold needed to support synaptic vesicle cycling--the process by
which brain cells release neurotransmitters to communicate with each other. The scientists blocked glycolysis, another way that cells make ATP,
so that the cells had to rely solely on their mitochondria for energy. This allowed the researchers to more accurately assess the contribution of mitochondrial ATP to different steps in the cycle,
and how this process goes awry when mitochondria malfunction. From this exploration, the scientists revealed that bringing the vesicles back up into the cell after they have released their neurotransmitters is the most energy-demanding process.
Indeed in the model of Leigh's disease, the cells did not have enough ATP to complete this step.
The researchers also compared energy levels in boutons--the docks from which neurotransmitters are shipped--with and without mitochondria.
Remarkably, there was no difference in energy levels between the two, and both types of boutons had sufficient ATP to support synaptic vesicle cycling.
From this, the scientists concluded that under normal conditions, ATP diffuses rapidly from boutons with mitochondria to those without,
so that even those boutons lacking mitochondria have sufficient energy to function under normal conditions. They note it will be important to determine
if boutons lacking mitochondria will still be able to function properly in diseases that disrupt the distribution of mitochondria.
"We really need to understand the basics of cell biology in a normal setting in order to comprehend changes in disease,
"he explains.""It's worth taking the time to study these underlying biological processes so that we can identify the best therapeutic targets for neurodegenerative disorders
#Whole genome-sequencing uncovers new genetic cause for osteoporosis Using extensive genetic data compiled by the UK10K project,
an international team of researchers led by Dr. Brent Richards of the Lady Davis Institute at the Jewish General Hospital has identified a genetic variant near the gene EN1 as having the strongest effect on bone mineral density (BMD)
and fracture identified to date. The findings are published in the forthcoming issue of the journal Nature."
"EN1 has never before been linked to osteoporosis in humans, so this opens up a brand new pathway to pursue in developing drugs to block the disease,"Dr. Richards,
an Associate professor of Medicine at Mcgill University, says by way of explaining the importance of the discovery."
"The effect of this uncommon genetic variant that we identified in this gene is twice as large as any previously identified genetic variants for BMD
and fracture,"adds Vince Forgetta, first author on this collaborative project from the Genetic Factors for Osteoporosis Consortium,
and a Research Associate at the Lady Davis Institute. Osteoporosis is a common disease that will lead to fractures in between one-third and one-half of all women over the course of their lives.
Because osteoporosis becomes more severe with age, it is becoming more prevalent with the overall aging of the population.
There are currently few safe and effective treatments for osteoporosis and no curative therapies available. The UK10K project has measured genetic variations in 10,000 individuals in great detail,
allowing researchers to correlate rare genetic changes with human disease by comparing the DNA of healthy individuals with those who have health problems.
The use of such an extensive sample size allows for the observation of genetic variants that are not discernable among smaller groups.
This particular study also stands as proof of principle that uncommon genetic variants can have a significant impact on common diseases."
"The hypothesis is that the genetic sequencing being done by UK10K will expose previously unknown genetic factors underlying disease,
"said Dr. Celia Greenwood, a biostatistician who is Senior Investigator at the Lady Davis Institute and Associate professor at Mcgill University,
and cochaired the statistics group for a companion Nature article on the methodology behind UK10K."
"We are finally able to extract enough data to discern variants that are rare in the overall population
and are more frequent among those with common diseases. This is precisely what has been revealed in the case of EN1
and osteoporosis."This study represents an initial realization of the hope that accompanied the development of genetic sequencing technology:
that sophisticated analysis of the genome would reveal those genes associated with disease. The promise for the contribution genetics can make to human health lies in the discovery of novel compounds that can counter the effect of deleterious genetic variants influencing these genes s
#Research breakthrough in fight against muscle wasting diseases It is estimated that half of all cancer patients suffer from a muscle wasting syndrome called cachexia.
Cancer cachexia impairs quality of life and response to therapy, which increases morbidity and mortality of cancer patients.
Currently, there is no approved treatment for muscle wasting but a new study from the Research Institute of the Mcgill University Health Centre (RI-MUHC) and University of Alberta could be a game changer for patients, improving both quality of life and longevity.
The research team discovered a new gene involved in muscle wasting that could be a good target for drug development.
The findings which were published in September's print edition of the FASEB Journal (Federation of American Societies for Experimental biology),
could have huge clinical implications, as muscle wasting is associated also with other serious illnesses such as HIV/AIDS, heart failure,
rheumatoid arthritis and chronic obstructive pulmonary disease and is also a prominent feature of aging.""We discovered that the gene USP19 appears to be involved in human muscle wasting and that in mice, once inhibited,
it could protect against muscle wasting, ''says lead author Dr. Simon Wing, MUHC endocrinologist and professor of Medicine at Mcgill University."
"Muscle wasting is a huge unmet clinical need. Recent studies show that muscle wasting is much more common in cancer than we think."
"In this study, researchers created mice models that were lacking USP19 (USP19 KO for''knockout''mice)
and decided to look at two common causes of muscle wasting. They observed whether such mice were resistant to muscle wasting induced by a high level of cortisol--a stress hormone released in your body any time you have a stressful situation such as an illness or a surgery.
They also looked at the loss of nerve supply because muscle atrophy can occur following a stroke
when people are weak and bedbound. In addition, they looked at USP19 levels in human muscle samples from the most common cancers that cause muscle wasting:
lung and gastrointestinal (pancreas, stomach, and colon.""We found that USP19 KO mice were wasting muscle mass more slowly;
''explains Dr. Wing who is also the director of the Experimental Therapeutics and Metabolism Program at the RI-MUHC."
and other biomarkers that reflect muscle wasting.''''According to recent studies, the prevalence of cachexia is high,
ranging from 5 to 15 per cent in chronic heart failure and COPD, and from 60 to 80 per cent in advanced cancer.
In all of these chronic conditions, muscle wasting predicts earlier death.""Cancer patients often present with muscle wasting even prior to their initial cancer diagnosis,
''says Dr. Antonio Vigano, director of the cancer rehabilitation program and cachexia clinic at the MUHC."
"In cancer, cachexia also increases your risk of developing toxicity from chemotherapy and other oncological treatments, such as surgery and radiotherapy.
At the Mcgill Nutrition and Performance Laboratory we specialize in cachexia and sarcopenia. By treating these two pathologic conditions through inhibiting the USP19 gene, at an early,
rather than late, stage of the cancer trajectory, not only can we potentially improve the quality of life of patients,
but also allow them to better tolerate their oncological treatments, to stay at home for a longer period of time,
and to prolong their lives
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