Synopsis: Domenii:


www.technology.org 2015 10193.txt.txt

#Polymer mold makes perfect silicon nanostructures Using molds to shape things is as old as humanity.

In the Bronze age, the copper-tin alloy was melted and cast into weapons in ceramic molds.

Today, injection and extrusion molding shape hot liquids into everything from car parts to toys.

For this to work, the mold needs to be stable while the hot liquid material hardens into shape.

In a breakthrough for nanoscience, Cornell polymer engineers have made such a mold for nanostructures that can shape liquid silicon out of an organic polymer material.

This paves the way for perfect 3-D, single crystal nanostructures. The advance is from the lab of Uli Wiesner, the Spencer T. Olin Professor of Engineering in the Department of Materials science and engineering,

whose lab previously has led the creation of novel materials made of organic polymers. With the right chemistry, organic polymers self-assemble,

and the researchers used this special ability of polymers to make a mold dotted with precisely shaped and sized nanopores..

Normally, melting amorphous silicon, which has a melting temperature of about 2, 350 degrees, would destroy the delicate polymer mold,

which degrades at about 600 degrees. But the scientists, in collaboration with Michael Thompson, associate professor of materials science and engineering, got around this issue by using extremely short melt periods induced by a laser.

The researchers found the polymer mold holds up if the silicon is heated by laser pulses just nanoseconds long.

At such short time scales, silicon can be heated to a liquid, but the melt duration is so short the polymer doesn have time to oxidize

and decompose. They essentially tricked the polymer mold into retaining its shape at temperatures above its decomposition point.

When the mold was etched away, the researchers showed that the silicon had been shaped perfectly by the mold.

This could lead to making perfect, single-crystal silicon nanostructures. They haven done it yet,

but their Science paper shows it possible. In work published in 2010, Wiesner and colleagues showed the pathway for this process,

using an oxide mold. Wiesner called the breakthrough eautifuland a possibly fundamental insight into studying nanoscale materials.

In materials science, the goal is always to get well-defined structures that can be studied without interference from material defects.

Most self-assembled nanostructures today are either amorphous or polycrystalline made up of more than one piece of a material with perfect order.

It hard to judge whether their properties are due to the nanostructure itself or whether theye dominated by defects in the material.

Discovery of single-crystal silicon the semiconductor in every integrated circuit made the electronics revolution possible.

It took cutting single crystals into wafers to truly understand silicon semiconducting properties. Today, nanotechnology allows incredibly detailed nanoscale etching, down to 10 nanometers on a silicon wafer.

But nanofabrication techniques like photolithography, in which a polymeric material is written with a structure that is etched into the silicon,

hits its limits when it comes to 3-D structures. Semiconductors like silicon don self-assemble into perfectly ordered structures like polymers Do it almost unheard of to get a 3-D structured single crystal of a semiconductor.

To make single crystal nanostructures there are two options: multiple etching or molding. Wiesner group now has made the mold.

The way they made the mold was itself a breakthrough. They had learned previously to self-assemble highly ordered,

porous nanomaterials using specially structured molecules called block copolymers. They first used a carbon dioxide laser in Thompson lab to ritethe nanoporous materials onto a silicon wafer.

A film, spin-coated on the wafer, contained a block copolymer, which directed the assembly of a polymer resin.

Writing lines in the film with the laser, the block copolymer decomposed, acting like a positive-tone resist,

while the negative-tone resin was left behind to form the porous nanostructure. That became the mold. e demonstrated that we can use organic templates with structures as complicated as a gyroid, a periodically ordered cubic network structure,

and mprintit onto molten silicon, which then transforms into crystalline silicon, Wiesner said. aving the ability to mold the workhorse of all electronics, silicon,

into intricate shapes is unprecedented, said Andy Lovinger, a program director in the materials research division at the National Science Foundation,

which funded Wiesner research. his beautiful work shows how it could be done by taking advantage of the unique design properties offered by polymeric materials. r


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#Pioneering gene therapy takes aim at inherited blindness Canada first human gene therapy trial for eyeshe replacement of a faulty gene with a healthy ones now underway at the Royal Alexandra Hospital to preserve

and potentially restore vision for people with a genetic disorder that leaves them blind by middle age. t a great privilege to be able to do something very positive for people with choroideremia,

says Ian Macdonald, a professor of ophthalmology with the Faculty of medicine & Dentistry at the University of Alberta,

and clinical research team leader. eople have hoped for this for a long time. horoideremia is a form of inherited blindness that affects one in 50,

000 people, about 90 per cent of whom are men. Many experience difficulty seeing at night during their teens, lose peripheral vision in adulthood

and are often legally blind by the age of 40. The disease is caused by a faulty gene that results in the degeneration of the light-sensing retinal cells at the back of the eye.

Until now, it has been untreatable. Gene therapy is not a drug, but a transfer of human genes.

Gene therapy refers to the incorporation of new DNA into cells, to replace a gene that is either missing or not functioning.

This allows the cells to produce an important protein. In choroideremia this protein is produced not

and retinal cells die off over time, causing vision to deteriorate. Macdonald trial involves a new treatment intended to stop choroideremia in its tracks with a single injection of

what known as a viral vector small harmless virus that been modified to carry into the eye the oodgene needed to potentially prevent further loss of sight

a surgeon detaches the area to be injected in the patient retina, then injects the viral vector through a narrow needle into the back of the eye.

The injection carries about 10 billion viral particles, each carrying a working copy of the good CHM gene,

replacing the defective gene that in the cells. he first of six local men to undergo ocular gene therapy,

I was sitting on a ship balcony thinking his is just my lot in life.

I got the call that I qualified for the surgery. he viral vector, known as AAV2-REP1, was provided by Nightstarx Ltd.,

a private British biopharmaceutical company focused on the development of therapies for retinal dystrophies. e are leading the way in the development of an effective gene therapy treatment for choroideremia,

and this new study sponsored by the University of Alberta is another step forward in the development of AAV2-REP1,

and the data to date have shown very promising results. he first clinical trials took place at the University of Oxford.

Oxford research is ongoing under the direction of ophthalmologist Robert Maclaren. Funds, support and equipment for the Canadian trial have been provided by various governmental and private agencies,

Alberta Innovates (Alberta Innovation and Advanced education), The Foundation Fighting Blindness, Choroideremia Research Foundation Canada, and private donors.

Researchers believe this new approach to eye therapy has promise for treating people early on before too many cells in the retina have been lost.

It may also have relevance for other, far more common causes of blindness, such as retinitis pigmentosa and age-related macular degeneration. f we can maintain the vision our patients have,

we would look at that as a success, says Chan. f there is improvement, that even better. acdonald says he bsolutely impressedby the eye ability to heal itself

and reattach the retina within hours of surgery. he human body is doing its work. Wee just helping it. ource:

University of Albert e


www.technology.org 2015 10206.txt.txt

#TSRI and Biotech Partners Find New Antibody Weapons against Marburg virus A new study led by scientists at The Scripps Research Institute (TSRI) identifies new immune molecules that protect against deadly Marburg virus, a relative

of Ebola virus. The research provides ingredients needed to develop treatments for future Marburg outbreaks. The team found antibodies (as above) that identify

and neutralize Marburg virushich inflicts a mortality rate of up to 90 percent. hese antibodies attack a new site on Marburg virus we had seen not before,

said Erica Ollmann Saphire, senior author of the new study, professor at TSRI and director of the Viral Hemorrhagic fever Immunotherapeutic Consortium.

The new antibodies that identify and neutralize Marburg virushich has a mortality rate of up to 90%ere developed through an academic-industrial partnership including TSRI, Integrated Biotherapeutics, Mapp Biopharmaceutical and Emergent biosolutions.

Currently, there are no vaccines or treatments specifically for Marburg infections. The findings were published online ahead of print today in the journal Plos Pathogens.

New Tools to Fight Marburg Virusthe new study builds on previous work in Saphire lab revealing a molecular structure that Marburg virus uses to attach to

and enter host cells. To defeat Marburg virus, scientists are looking for vulnerable sites on the virus surface where an antibody can bind.

Previous research, including trials with the experimental ZMAPPTM treatment shows that mixtures or ocktailsof antibodies can block Ebola virus from infecting new cells and alert the immune system to the presence of the infection.

It thought that a similar cocktail strategy could work against Marburg virus. Antibodies against one site on Marburg were revealed in a study by Vanderbilt University and TSRI in February 2015,

but complementary antibodies needed against other sites remained to be discovered. In the new study, TSRI researchers designed proteins which elicited new antibodies developed at Emergent biosolutions.

Other antibodies in the study were identified independently at Mapp Biopharmaceutical and Integrated Biotherapeutics which collaborated with TSRI for molecular analysis. Some of the new antibodies target a new site on Marburg virus not seen before winglike feature attached to the base of the virus. Antibodies against this newly discovered site protected 90 to 100%of infected animal models from lethal infection.

Ebola virus Also Vulnerablesome antibodies discovered in the new study are also able to cross-react with Ebola virus

and its four relatives in the Ebolavirus genus. e expect both Marburg virus and Ebola virus to emerge again

and to acquire new mutations, said TSRI Research Assistant Marnie Fusco, first author of the new study. he cross-reactive antibodies could be used as diagnostics for newly emerging strains.?

The high cost of creating independent vaccines or treatments for each of the different viruses in this family necessitates intelligent design of immunogens (antibody-inducing molecules).

The molecular images used to design the molecules and evaluate the antibodies point the way forward, added Jody Berry, the former Director of Pipeline Research of Emergent biosolutions,

who initiated the study with Saphire six years ago. nderstanding where and how the antibodies interact with the virus tells us which regions can be targeted

and helps us develop lead candidates for clinical development, said Cory Nykiforuk, current director of pipeline research of Emergent biosolutions. here are multiple filoviruses that threaten our communities, front line medical workers and defense personnel,

and bringing new technologies to the forefront could potentially help meet future requirements. ource: NSF, Scripps Research Institut r


www.technology.org 2015 10220.txt.txt

#Say It With Light: Using LEDS to Move Data Faster It like using fiber optics to communicate only without the fiber.

Imagine connecting to the Internet through the same room lights that brighten your day. A University of Virginia engineering professor and her former graduate student are already there.

Maite Brandt-Pearce, a professor in the Charles L. Brown Department of Electrical and Computer engineering,

and Mohammad Noshad, now a postdoctoral fellow in the Electrical engineering Department at Harvard university, have devised a way of using light waves from light-emitting diode fixtures to carry signals to wireless devices at 300 megabits per second from each light.

It like having a whole wi-fi system all to yourself; using light waves, there would be more network access points than with radio waves,

so less sharing of the wireless network. e developed a modulation algorithm that increases the throughput of data in visible light communications,

Brandt-Pearce said. e can transmit more data without using any additional energy. As more light fixtures get replaced with LED LIGHTS,

you can have different access points to the same network. Their breakthrough means that data can be transmitted faster with light waves using no more energy than is required already to run the lights.

Noshad, 29, from Iran started working with Brandt-Pearce on wireless optical communications in spring 2011

when he joined the electrical engineering department to pursue his Ph d. He received several prizes for his work

and earned his doctoral degree from U. Va. in 2013. e came up with the idea together,

we wrote the research papers together, and so it makes sense that we wanted the names of both professor and student on the patent,

Brandt-Pearce said. Noshad and Brandt-Pearce have filed a patent along with the University on their idea and Noshad has created a company,

VLNCOMM, for Visible light Network Communications, to which Brandt-Pearce is a consultant. The Charlottesville-based firm is developing a prototype for potential investors a desk lamp that provides an Internet connection through light

and conducting further research. Jie Lian, another one of Brandt-Pearce graduate students who has finished his master degree in electrical engineering

and is working toward a Ph d, . is focusing his research on multiuser systems, getting several lights to cooperate to send data to many users in a room,

making sure the lighting is good and everybody has a good connection. e have a patent with the University

and we will file more patents on the research being done now, Noshad said. e can make different products,

such as a large LED panel for shopping centers, airports and conference rooms. And we can build LED bulbs for use in the home.

He said it would be a matter of simply adding software to computers to connect them with LED transmitters. his is not a replacement for wi-fi;

it an augmentation, Brandt-Pearce said. esearchers have called it i-Fi Our modulation can be used in any optical device so this has the potential for widespread use

and much better access than present wi-fi based on radio waves. The firm, which has been in business since last year, employs about four people and Fraidoon Hovaizi,

an early investor, is president of the operation. VLNCOMM has drawn attention from venture capitalists and has gotten some funding from a federal Small Business Innovation Research program through the Federal department of Energy.

Noshad said the firm has gotten additional funding from the National Science Foundation and he thinks there may be more DOE funding for it in the near future. he idea in this technology is to transmit the data using the lighting systems that are used already for the illumination of indoor environments,

Noshad said. Visible light communications offer a compact, dual-use, energy saving solution and can provide a high-speed secure network connection for a large number of users.

Part of its value is in its versatility. ou can use it any place that has lighting,

Brandt-Pearce said. n a stadium, in a parking lot, or from vehicle to vehicle if using LED headlights and taillights.

Like current wireless communications, encryption is necessary to keep data secure but Brandt-Pearce noted that a secure network could be created in a room with no windows. t can be detected outside the room

because the light waves stop when they hit something opaque, such as a wall, she said. hat can keep communications secure from room to room.

And two separate networks in different rooms would not interfere with each other the way they do with present wi-fi networks.

She said devices with LED circuits in them can also communicate with each other. our alarm clock can communicate with your coffee maker that it is time to start making the coffee

she said. nything with an LED can talk to anything else with an LED. You don need a separate transmitter

because you are not using radio waves. And because it does not use radio waves, this system can be used in places where radio waves could create problems,

such as in hospitals, in manufacturing facilities and in airplane cabins. Visible light communications has the potential to significantly increase the speed of Internet connection in multiuser indoor environments due to the broad bandwidth of the visible light,

Noshad said. t will offer a huge energy saving for the nation since energy is used already for lighting,

and thus does need not to be expended for communications. Noshad said that some experts have forecast the LED communications market at $6 billion by 2020. here are people working on it in Asia and Europe,

he said. believe this is going to be a big market. Brandt-Pearce, who has taught at U. Va. School of engineering

and Applied science for 22 years, said the visible light communications project is one of about four or five on

which she is working simultaneously. Others include determining how much data can be pushed through an optical fiber

and how to design long-haul fiber-optic networks so the data quality stays high while the data throughput is increased. like that each day is different

and that there are different projects to work on, she said. love my job because I am having fun doing it,

and still making a difference in people lives. Source: University of Virgini


www.technology.org 2015 10229.txt.txt

#Elastic Gel to Heal Wounds A team of bioengineers at Brigham and Women Hospital (BWH), led by Ali Khademhosseini, Phd,

and Nasim Annabi, Phd, of the Biomedical engineering Division, has developed a new protein-based gel that,

when exposed to light, mimics many of the properties of elastic tissue, such as skin and blood vessels.

In a paper published in Advanced Functional Materials, the research team reports on the new material key properties, many

of which can be tuned finely, and on the results of using the material in preclinical models of wound healing. e are interested very in engineering strong,

elastic materials from proteins because so many of the tissues within the human body are elastic. If we want to use biomaterials to regenerate those tissues,

we need elasticity and flexibility, said Annabi, a co-senior author of the study. ur hydrogel is made very flexible

from a biocompatible polypeptide and can be activated using light. ydrogels jellylike materials that can mimic the properties of human tissue are used widely in biomedicine,

but currently available materials have limitations. Some synthetic gels degrade into toxic chemicals over time,

and some natural gels are not strong enough to withstand the flow of arterial blood through them,

said Khademhosseini. The new material, known as a photocrosslinkable elastin-like polypeptide-based (ELP) hydrogel, offers several benefits.

This elastic hydrogel is formed by using a light-activated polypeptide. When exposed to light, strong bonds form between the molecules of the gel,

providing mechanical stability without the need for any chemical modifiers to be added to the material.

The team reports that ELP hydrogel can be digested overtime by naturally-occurring enzymes and does not appear to have toxic effects

when tested with living cells in the lab. The team also found that they could control how much the material swelled as well its strength,

finding that the ELP hydrogel could withstand more stretching than experienced by arterial tissue in the body. ur hydrogel has many applications:

it could be used as a scaffold to grow cells or it can be incorporated with cells in a dish

and then injected to stimulate tissue growth, said Annabi. n addition, the material can be used as a sealant,

sticking to the tissue at the site of injury and creating a barrier over a wound.

The researchers found that it was possible to combine the gel with silica nanoparticles microscopic particles previously found to stop bleeding to develop an even more powerful barrier to promote wound healing. his could allow us to immediately stop bleeding with one treatment

said Annabi. e see great potential for use in the clinic. Our method is simple,

the material is biocompatible, and we hope to see it solve clinical problems in the future. Further investigation in preclinical models will be needed to test the material properties and safety before approval for use in humans e


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#Researchers show that telomeres are linked to the origins of idiopathic pulmonary fibrosis Samples from mouse lungs show collagen fibers that generate pulmonary fibrosis.

These results suggest that idiopathic pulmonary fibrosis may be treated by therapies based on the activation of the enzyme telomerase.

Idiopathic pulmonary fibrosis (IPF) causes a gradual loss of respiratory capacity and can be lethal within a few years.

The cause is unknown, although it can be attributed to a combination of genetics and the environment.

A team of researchers from the Spanish National Cancer Research Centre (CNIO) have discovered now that telomeres

the structures that protect the chromosomes, are at the origin of pulmonary fibrosis. This is the first time that telomere damage has been identified as a cause of the disease.

This finding opens up new avenues for the development of therapies to treat a disease for

which there is currently no treatment. This work, carried out by Juan M. Povedano and Paula Martínez from the Telomeres and Telomerase Group at CNIO led by Maria A. Blasco,

with the participation of researchers from the CNIO Molecular Imaging Core Unit and from the Complutense University of Madrid, is being published this week in the journal Cell Reports.

Idiopathic pulmonary fibrosis is a respiratory disease? affecting about 8, 000 people in Spain? in which scars are formed in lung tissue that make it rigid, leading to breathing difficulties.

In the absence of a single and determinant cause, researchers compile clues that piece together different parts of the problem.

One is that the exposure to environmental hazards, such as radiation, smoking or pollution, greatly increases the risk.

Other clues already pointed to the telomeres. For example, the telomeres of many patients suffering from idiopathic pulmonary fibrosis are shorter than normal.

Furthermore, pulmonary fibrosis is one of the most frequent illnesses among people with mutations in genes involved in telomere maintenance.

These data suggest that there is an association between telomere defects and the disease but demonstration of causation was pending.

TELOMERE DEFECTS In search of a cause-effect relationship, CNIO researchers created a mouse that lacked a protein needed to build telomeres in a specific cell population type II alveolar cells and

which is indispensable for lung tissue regeneration. The results left no room for doubt: most of the animals developed progressive pulmonary fibrosis.

The researchers, after finding that the lack of telomeres is lethal for type II alveolar cells,

reached the conclusion that lung epithelium cannot regenerate without these cells and, therefore, cannot repair damage caused by toxic environmental agents.

This result demonstrates, for the first time, that telomere damage may cause pulmonary fibrosis. In the words of Martínez:

e have seen that acute telomere damage is sufficient to trigger pulmonary fibrosis, even in the absence of environmental damage.

A MODEL THAT REPRODUCES THE DISEASE IN HUMANS Although the mouse lacking telomeres in pulmonary epithelial cells proves the importance of telomeres in the origin of fibrosis,

it does not however reproduce the disease in most human patients. In humans, environmental hazards play an important role in the disease.

Furthermore, short telomeres are also a feature of the disease. Very short telomeres are a permanent damage to cells

and they stop dividing. When this happens, pulmonary tissue will cease to regenerate and instead, a rotectiveprogramme against damage will be triggered that causes scar formation

which leads to fibrosis. The researchers therefore developed an animal model that combines premature shortening of the telomeres due to telomerase deficiency, with low doses of environmental damage.

To induce damage they chose bleomycin, a drug that affects the genetic material of cells and inhibits cell division

when administered in high doses, but not enough to cause pulmonary fibrosis in normal mice at the low doses administered by the authors.

They saw that there is a synergy between the damage caused by bleomycin at low doses

and the one caused by short telomeres. The shortening of the telomeres is not in itself sufficient to generate fibrosis

nor, in general, is bleomycin at low doses; however, both factors together do trigger the disorder. hese findings support a model in

which persistent damage derived from short or dysfunctional telomeres is added to other cellular damage and this triggers pulmonary fibrosis, says Povedano.

The new animal models are essential for testing new herapeutic strategies based on the activation of telomerase the enzyme that repairs telomeres,

concludes the paper in Cell Reports. A LINK TO AGEING This new evidence, which focuses on telomeres,

fits in well with the fact that idiopathic pulmonary fibrosis only occurs in people over 50 years of age;

it is precisely in the telomeres where one of the main molecular symptoms of cellular ageing occurs.

Telomeres become shorter each time a cell divides; the older the organism, the greater the number of divisions and the shorter the telomeres.

Blasco asserts: nderstanding the molecular mechanisms that lead to the ageing process, such as the shortening of telomeres, has enabled us to generate animal models that faithfully reproduce diseases such as idiopathic pulmonary fibrosis,

and this is already helping us to test novel therapies that we hope will prove effective

and that are based on the activation of the enzyme telomerase. n


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