Nanoscale Speed bump Could Regulate Plasmons for High-speed data Flow The name sounds like something Marvin the Martian might have built,
Developed by a team of government and university researchers, including physicists from the National Institute of Standards and Technology (NIST),
the innovation harnesses tiny electron waves called plasmons. It a step towards enabling computers to process information hundreds of times faster than today machines.
Computers currently shuttle information around using electricity traveling down nanoscale metal wires. Although inexpensive and easy to miniaturize,
metal wires are limited in terms of speed due to the resistance in the metal itself. Fiber optics use light to move information about 10
000 times faster, but these and other nonmetallic waveguides are constrained by pesky physical laws that require critical dimensions to be at least half the wavelength of the light in size;
still small, but many times larger than the dimensions of current commercial nanoscale electronics. Plasmonics combines the small size and manufacturability of electronics with the high speeds of optics.
When light waves interact with electrons on a metal surface, strong fields with dimensions far smaller than the wavelength of the original light can be createdlasmons.
Unlike light, these plasmons are free to travel down nanoscale wires or gaps in metals.
The team, which included researchers from Rutgers, the University of Colorado at Colorado springs, and Argonne National Laboratory, fabricated their device using commercial nanofabrication equipment at the NIST Nanofab.
Small enough to serve in existing and future computer architectures this technology may also enable electrically tunable and switchable thin optical components.
Their findings were published in Nature Photonics.**The plasmonic phase modulator is inverted effectively an, nanoscale speed bump.
Eleven gold strands are stretched side by side like footbridges across a 23-micrometer gap just 270 nanometers above the gold surface below them.
Incoming plasmons, created by laser light at one end of the array, travel though this air gap between the bridges and the bottom gold layer.
When a control voltage is applied, electrostatic attraction bends the gold strands downwards into a U shape.
At a maximum voltagelose to the voltages used in today computer chipshe gap narrows, slowing the plasmons.
As the plasmons slow their wavelength becomes shorter, allowing more than an extra half of a plasmonic wave to fit under the bridge.
Because it exactly out of phase with the original wave, this additional half wavelength can be used to selectively cancel the wave,
making the bridge an optical switch. At 23 micrometers, the prototype is relatively large, but according to NIST researcher Vladimir Aksyuk, their calculations show that the device could be shortened by a factor of 10,
scaling the device footprint down by a factor of 100. According to these calculations, the modulation range can be maintained without increase in the optical loss
as the length and the size of the gap are reduced. ith these prototypes, we showed that nanomechanical phase tuning is efficient,
says Aksyuk. his effect can be generalized to other tunable plasmonic devices that need to be made smaller.
you can put more of them on the same chip, bringing them closer to practical realization. i
#Study finds cystic fibrosis decreases muscle strength Patients with cystic fibrosis have a muscle deficiency that gets worse with age, according to the findings of a joint study by researchers at the University of Georgia and Georgia Regents University.
The study, conducted as a partnership between the kinesiology department at the UGA College of Education
and Georgia Regents University, measured the oxygen capacity of muscles in patients age 7-42.
and results showed cystic fibrosis patients had 15 percent less capacity than the control group -and that capacity grew worse with age.
Cystic fibrosis is a genetic disease that primarily affects the lungs and digestive system of about 30,000 Americans, producing mucus that makes it difficult to breathe
The average life span of a patient with cystic fibrosis is less than 40 years. By including children in the study,
researchers opened a door to similar tests on a range of childhood diseases. The Mito Test uses near infrared spectroscopy, a special type of light beamed through the skin
to measure the oxygen levels in muscle mitochondria. Because it is a noninvasive test relying on sensors placed on the skin,
it is easier to administer than traditional methods to measure muscle capacity, such as MRIS or biopsies.#
#This is the first time we could test on children, which is groundbreaking for us, #said Kevin Mccully, one of the authors of the study and a professor in the UGA College of Education#s kinesiology department.#
#We did find there was evidence of muscle impairment, and it gets worse the older you get.
points to this decrease of muscle strength as one reason why cystic fibrosis patients are less likely to exercise as they get older,
complicating their health problems. Mccully, who developed the Mito Test, said the excessive muscle weakness that is common in cystic fibrosis patients now can be attributed to some degree to defects in muscle mitochondria.
Mccully and other UGA researchers will continue to work with Georgia Regents University to determine what is keeping cystic fibrosis patients#muscles from properly functioning,
as well as use the Mito Test in Athens, Augusta and elsewhere to study other childhood diseases that may affect muscle mitochondria.#
#This is the start of a collaboration; we agree there is something in the muscles that accumulates,
noting the shortened life span of cystic fibrosis patients.##We#re interested in optimizing that life,
University of Georgi r
#New treatment options for colon cancer Scientists from Nanyang Technological University (NTU) and Sweden Karolinska Institutet, one of Europe largest and most prestigious medical universities, have discovered that an existing
chemotherapy drug used to treat leukaemia could prevent and control the growth of colorectal tumours. Colorectal cancer commonly referred to as colon cancer is one of the three most common cancers worldwide and the most common in Singapore.
Almost 95 per cent of colorectal cancers are from malignant tumours. The research team found that Imatinib,
an enzyme blocker widely used to treat leukaemia, works by blocking a signalling pathway related to a group of cell receptors called Ephb.
This means that when used to treat mice with colon tumours it was able to halve the growth of tumours in the intestines.
The finding is also significant as currently there is no drug available to prevent the recurrence of tumours in the intestine after the cancerous tumours have been removed by surgery.
One of the two principal investigators in the team of 13 international scientists was Prof Sven Pettersson,
Professor of Metabolic Disease at NTU Lee Kong Chian School of medicine and senior principal investigator with the National Cancer Centre Singapore. ur work has important clinical implications,
and cancer progression in patients predisposed to develop colorectal cancer, said Prof Pettersson, who is also a Professor of Host-Microbe Interactions at Karolinska Institutet.
Dr Parag Kundu, a senior research fellow with Prof Pettersson lab and the first author of the study, said that in their tests,
which had late-stage tumours and rectal bleeding. The same effects were shown also when Imatinib was tested on colon tumour tissues taken from human patients.
where the affected section of the intestine is removed through surgery. The scientists said these findings also suggest that short term intermittent chemotherapies could be possible as a treatment model,
Professor of Stem Cell Research at Karolinska Institutet, who co-supervised the study. This is beneficial as Ephb receptors also function to keep the tumour intact,
#Unusual Chance to Study Patient's Residual Tumor Leads to New Finding Capitalizing on a rare opportunity to thoroughly analyze a tumor from a lung cancer patient who had developed resistance to targeted drug treatment,
UC San francisco scientists identified a biological escape hatch that explains the resistance, and developed a strategy in mice for shutting it down.
the researchers were able to durably wipe out cancer cells in mice implanted with cells from the drug-resistant tumor. ven in cancers that are responding to targeted therapy by conventional criteria,
the senior author of the new study, Trever Bivona, MD, Phd, assistant professor of medicine and member of the UCSF Helen Diller Family Comprehensive Cancer Center (HDFCCC).
n this work we have begun to crack open the question of why residual disease persists after targeted therapy.
Between 10 and 35 percent of non-small cell lung cancer (NSCLC) patients carry mutations in a gene that codes for a cell-surface protein called the epidermal growth factor receptor, or EGFR.
But the EGFR mutations seen in NSCLC cause the receptor to be stuck in an nposition, leading to rampant cell proliferation.
which drug-resistant cells that survive treatment form residual, often lethal, tumors. Understanding the biological basis of acquired resistance has proved difficult,
partly because patients with late-stage lung cancer rarely undergo surgery, leaving scientists with few drug-resistant tumors to use in research.
But as described in the online edition of Cell Reports on Thursday, April 2, 2015, a team of UCSF researchers recently had unusual access to a surgically resected tumor from an EGFR-mutant lung cancer patient who had experienced a substantial,
but incomplete, response to erlotinib. Led by first authors Collin Blakely, MD, Phd, a clinical instructor at UCSF,
and Evangelos Pazarentzos, Phd, a postdoctoral fellow, the research group analyzed cells from this tumor using next-generation genome sequencing in an effort to understand how the cells sidestepped erlotinib treatment.
They found that the tumor cells retained the EGFR mutation targeted by erlotinib and had acquired not additional cancer-driving mutations,
or any other mutations known to confer drug resistance. These results suggested that the cells were still potentially susceptible to erlotinib,
but had enlisted some additional mechanism to survive treatment. That mechanism was revealed when cells from the tumor were implanted in mice that were treated then with erlotinib.
The drug effectively inhibited EGFR activity, but the researchers also observed a rapid, 10-fold increase in the activity of a pathway known as NF-KAPPA-B,
and they discovered that this increase is mediated by a previously unknown biochemical complex formed within the tumor cells.
Though primarily associated with the immune system a growing body of work has tied the NF-KAPPA-B pathway to various forms of cancer.
An experimental drug known as PBS-1086 directly targets the NF-KAPPA-B pathway, and when the researchers coupled this drug with erlotinib,
the implanted tumors shrank significantly, suggesting that combining a compound like PBS-1086 with erlotinib at the outset of therapy may help to prevent acquired drug resistance in EGFR-mutant NSCLC.
Combined drug regimens designed to overcome drug resistance at the outset of therapy are now the norm in treating certain forms of melanoma,
said Bivona, and he believes PBS-1086 as a shotto play a similar role in NSCLC. he NF-KAPPA-B pathway is engaged by cells in response to EGFR inhibitors as a way to survive treatment,
we see tumors shrink. In lung cancer patients treated with these drugs, and that a substantial number of patients, this could be a very powerful companion therapy to minimize
or eliminate residual disease. i
#Engineers gain control of gene activity; new therapies may be ahead Duke researchers have developed a new method to precisely control
when genes are turned on and active. The new technology allows researchers to turn on specific gene promoters
and enhancersieces of the genome that control gene activityy chemically manipulating proteins that package DNA.
This web of biomolecules that supports and controls gene activity is known as the epigenome. The researchers say having the ability to steer the epigenome will help them explore the roles that particular promoters
and enhancers play in cell fate or the risk for genetic disease and it could provide a new avenue for gene therapies
and guiding stem cell differentiation. he epigenome is associated everything with the genome other than the actual genetic sequence,
and is just as important as our DNA in determining cell function in healthy and diseased conditions,
assistant professor of biomedical engineering at Duke. hat becomes immediately obvious when you consider that we have over 200 cell types,
explained Gersbach. ut there also many other pieces of the genome called enhancers that aren next to any genes at all,
Timothy Reddy, assistant professor of biostatistics and bioinformatics at Duke, has spent the better part of a decade mapping millions of these enhancers across the human genome.
Reddy thought perhaps he could chemically alter the histones at the enhancers to turn them on. here are already drugs that will affect enhancers across the whole genome,
and modify very specific epigenetic marks in very specific places to find out what individual enhancers are doing.
Reddy found that specificity by teaming up with Gersbach, his neighbor within Duke Center for Genomic and Computational biology,
and paste DNA sequences in the human genome. For this epigenome editing application, Gersbach silenced the DNA-cutting mechanism of CRISPR
so that we can alter the DNA packaging at that specific site, said Reddy. Gersbach and Reddy put their artificial epigenetic agent to the test by targeting a few well-studied gene promoters and enhancers.
While these histone modifications have long been associated with gene activity it wasn clear if they were enough to turn genes on.
But the real excitement from their results is an emerging ability to probe millions of potential enhancers in a way never before possible. ome genetic diseases are straightforwardf you have a mutation within a particular gene,
then you have said the disease Isaac Hilton, postdoctoral fellow in the Gersbach Lab and first author of the study. ut many diseases, like cancer,
cardiovascular disease or neurodegenerative conditions, have a much more complex genetic component. Many different variations in the genome sequence can affect your risk of disease
and this genetic variation can occur in these enhancers that Tim has identified, where they can change the levels of gene expression.
With this technology, we can explore what exactly it is that theye doing and how it relates to disease or response to drug therapies.
Gersbach added, ot only can you start to answer those questions, but you might be able to use this technique for gene therapy to activate genes that have been silenced abnormally
or to control the paths that stem cells take toward becoming different types of cells.
These are all directions we will be pursuing in the future. e
#Star Pair#s Dusty Disk Shines Light on Planet formation Astronomers using the Gemini South telescope in Chile have discovered striking new evidence for planet formation in a dusty disk surrounding
a pair of stars in Sagittarius. The team took advantage of an offering for Early Science using the Gemini Planet Imager to study infrared light scattered off dust grains in the disk around the binary system V4046 Sgr.
where r is the distance in pixels from the central binary, corrected for projection effects. Both images are shown on a linear scale and oriented north up and east left.
where r is the distance in pixels from the central binary, corrected for projection effects. Both images are shown on a linear scale and oriented north up and east left.
Analysis of the data also indicates that the dust grains orbiting the star are sorted by particle size,
#Scientists discover new treatment for dementia Pushing new frontiers in dementia research, Nanyang Technological University,
Singapore (NTU Singapore) scientists have found a new way to treat dementia by sending electrical impulses to specific areas of the brain to enhance the growth of new brain cells.
Known as deep brain stimulation, it is a therapeutic procedure that is already used in some parts of the world to treat various neurological conditions such as tremors or Dystonia,
which mitigates the harmful effects of dementia-related conditions and improves short and long-term memory. Their research has shown that new brain cells,
which is involved in memory retention using minute amounts of electricity. The increase in brain cells reduces anxiety and depression,
and promotes improved learning, and boosts overall memory formation and retention. The research findings open new opportunities for developing novel treatment solutions for patients suffering from memory loss due to dementia-related conditions such as Alzheimer and even Parkinson disease.
This discovery was published in elife, a peer-reviewed open-access scientific journal published by the Howard hughes medical institute, the Max Planck Society and the Wellcome Trust.
Assistant professor Ajai Vyas from NTU School of Biological sciences said he findings from the research clearly show the potential of enhancing the growth of brain cells using deep brain stimulation. round 60 per cent of patients do not respond to regular antidepressant treatments
and our research opens new doors for more effective treatment options. Dr Lim Lee Wei, an associate professor at Sunway University, Malaysia, who worked on the research project
while he was a Lee kuan yew Research Fellow at NTU, said that deep brain stimulation brings multiple benefits. o negative effects have been reported in such prefrontal cortex stimulation in humans
and studies have shown that stimulation also produces anti-depression effects and reduces anxiety. emory loss in older people is not only a serious and widespread problem,
but signifies a key symptom of dementia. At least one in 10 people aged 60 and above in Singapore suffer from dementia
and this breakthrough could pave the way towards improved treatments for patients. Growing new brain cells For decades, scientists have been finding ways to generate brain cells to boost memory and learning,
but more importantly, to also treat brain trauma and injury, and age-related diseases such as dementia. As part of a natural cycle, brain cells constantly die
and get replaced by new ones. The area of the brain responsible for generating new brain cells is known as the hippocampus
which is involved also in memory forming, organising and retention. By stimulating the front part of the brain known as the prefrontal cortex,
new brain cells are formed in the hippocampus although it had not been stimulated directly. The research was conducted using middle-aged rats, where electrodes
which sends out minute micro-electrical impulses were implanted in the brains. The rats underwent a few memory tests before and after stimulation,
said Prof Ajai who is a recipient of NTU prestigious Nanyang Assistant Professorship award. he electrodes are harmless to the rats,
#Biologists identify brain tumor weakness Biologists at MIT and the Whitehead Institute have discovered a vulnerability of brain cancer cells that could be exploited to develop more-effective drugs against brain tumors.
The study, led by researchers from the Whitehead Institute and MIT Koch Institute for Integrative Cancer Research, found that a subset of glioblastoma tumor cells is dependent on a particular enzyme that breaks down the amino acid glycine.
Without this enzyme, toxic metabolic byproducts build up inside the tumor cells, and they die. GLDC caught the researchersattention as they investigated diseases known as nborn errors of metabolism
which occur when cells are missing certain metabolic enzymes. Many of these disorders specifically affect brain development;
the most common of these is marked phenylketonuria by an inability to break down the amino acid phenylalanine.
Such patients must avoid eating phenylalanine to prevent problems such as intellectual disability and seizures. Loss of GLDC produces a disorder called nonketotic hyperglycinemia,
which causes glycine to build up in the brain and can lead to severe mental retardation. GLDC is also often overactive in certain cells of glioblastoma,
the most common and most aggressive type of brain tumor found in humans. The researchers found that GLDC,
These regions are often found at the center of tumors, which are inaccessible to blood vessels.
It turns out that in this low-oxygen environment, SHMT2 gives cells a survival edge because it can indirectly influence the activity of an enzyme called PKM2,
but the same regulation also affects the consumption of oxygen a scarce resource in ischemic regions. ells that have high SHMT2 activity have low PKM2 activity,
which makes them better suited to survive in the ischemic tumor microenvironment, Kim says. However, this highly active SHMT2 also produces a glut of glycine,
Without GLDC, glycine enters a different metabolic pathway that generates toxic products that accumulate and kill the cell. n interesting aspect of the current study is uncovered that they why glycine accumulation is toxic,
says Navdeep Chandel, a professor of medicine and cellular biology at Northwestern University who was not part of the research team.
LDC loss accumulates glycine, causing nonketotic hyperglycinaemia, a disorder that severely affects the developing brain.
resulting in funneling of glycine into metabolic pathways that generate toxic molecules, such as aminoacetone and methylglyoxal.
#In first human study, new antibody therapy shows promise in suppressing HIV infection In the first results to emerge from HIV patient trials of a new generation of so-called broadly neutralizing antibodies,
Rockefeller University researchers have found the experimental therapy can dramatically reduce the amount of virus present in a patient blood.
The work, reported this week in Nature, brings fresh optimism to the field of HIV immunotherapy
and suggests new strategies for fighting or even preventing HIV infection. hiv antibodies In a person infected with HIV,
there is an ongoing arms race between the virus and the body immune system. Even as the body produces new antibodies that target the virus
the virus is constantly mutating to escape, managing to stay just a few steps ahead. The new study, conducted in Michel Nussenzweig Laboratory of Molecular Immunology,
finds that administration of a potent antibody, called 3bnc117, can catch HIV off guard and reduce viral loads.
HIV antibodies previously tested in humans had shown disappointing results. 3bnc117 belongs to a new generation of broadly neutralizing antibodies that potently fight a wide range of HIV strains. hat special about these antibodies is that they have activity against over 80 percent
of HIV strains and they are extremely potent, says Marina Caskey, assistant professor of clinical investigation in the Nussenzweig lab and co-first author of the study. 3bn117,
which was isolated originally by Johannes Scheid in the Nussenzweig laboratory, targets the CD4 binding site of the HIV envelope,
and the CD4 receptor is the primary site of attachment of HIV to host cells,
3bnc117 shows activity against 195 out of 237 HIV strains. Broadly neutralizing antibodies are produced naturally in some 10 to 30 percent of people with HIV,
but only after several years of infection. By that time the virus in their bodies has evolved typically to escape even these powerful antibodies.
However by isolating and then cloning these antibodies, researchers are able to harness them as therapeutic agents against HIV infections that have had less time to prepare.
Earlier work in the Nussenzweig lab had demonstrated that these potent antibodies could prevent or suppress infection in mouse and nonhuman primate models of HIV.
But these animal models are very rough approximations of human infections, explains Caskey. The mice must be engineered genetically to be susceptible to HIV
and therefore lack an intact immune system, and the primates used in HIV studies can only be infected with a simian version of the virus. The proof of principle awaited human trials.
In the new study uninfected and HIV-infected individuals were given intravenously a single dose of the antibody
and monitored for 56 days. At the highest dosage level tested in the study, 30 milligrams per kilogram of weight,
all eight infected individuals treated showed up to 300-fold decreases in the amount of virus measured in their blood,
with most reaching their lowest viral load one week after treatment. The drop in viral load depended on the individual starting viral load and also the sensitivity of their particular strains of HIV to the antibody.
This is the first time that the new generation of HIV antibodies has been tested in humans. Not only was a single dose of 3bn117 well tolerated and effective in temporarily reducing viral loads,
in some individuals it remained active in the body for a long time. In half of the individuals receiving the highest dose,
viral loads remained below starting levels even at the end of the 8-week study period and resistance to 3bnc117 did not occur.
Researchers also believe that antibodies may be able to enhance the patient immune responses against HIV, which can in turn lead to better control of the infection.
In addition, antibodies like 3bnc117 may be able to kill viruses hidden in infected cells, which serve as viral reservoirs inaccessible to current antiretroviral drugs.
Most likely 3bnc117, like other anti-retrovirals, will need to be used in combination with other antibodies
or antiretroviral drugs to keep infections under control. ne antibody alone, like one drug alone, will not be sufficient to suppress viral load for a long time
because resistance will arise, says Caskey. One important benefit is the dosing schedule: an antibody therapy for HIV might require treatment just once every few months,
compared to daily regimens of antiretroviral drugs that are now the front-line treatment for HIV. n contrast to conventional antiretroviral therapy,
antibody-mediated therapy can also engage the patient immune cells, which can help to better neutralize the virus,
says co-first author Florian Klein, also assistant professor of clinical investigation in the Nussenzweig laboratory.
Besides the possibility of treatment, the study also raises hopes for an HIV vaccine. If researchers can induce an uninfected person immune system to generate potent antibodies such as 3bnc117
it might be enough to block the HIV infection before it can be established. Ongoing clinical research in Nussenzweig lab and The Rockefeller University Hospital aims to address the impact of additional broadly neutralizing antibodies, alone or in combination, on viral load in HIV-infected patients.
Source: Rockefeller Universit l
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