University of California San Diego

New nano-implant could one day help restore sight

Posted by

0


New nano-implant could one day help restore sight
Scanning electron micrograph (SEM) image of individual nanowires and groupies of nanowires. Each wire can produce an electric current when hit by light.  

A team of engineers at the University of California San Diego and La Jolla-based startup Nanovision Biosciences Inc. have developed the nanotechnology and wireless electronics for a new type of retinal prosthesis that brings research a step closer to restoring the ability of neurons in the retina to respond to light. The researchers demonstrated this response to light in a rat retina interfacing with a prototype of the device in vitro.

 They detail their work in a recent issue of the Journal of Neural Engineering.  The technology could help tens of millions of people worldwide suffering from neurodegenerative diseases that affect eyesight, including macular degeneration, retinitis pigmentosa and loss of vision due to diabetes.

Despite tremendous advances in the development of over the past two decades, the performance of devices currently on the market to help the blind regain functional vision is still severely limited—well under the acuity threshold of 20/200 that defines legal blindness.

“We want to create a new class of devices with drastically improved capabilities to help people with impaired vision,” said Gabriel A. Silva, one of the senior authors of the work and professor in bioengineering and ophthalmology at UC San Diego.  Silva also is one of the original founders of Nanovision.

The new prosthesis relies on two groundbreaking technologies. One consists of arrays of silicon nanowires that simultaneously sense light and electrically stimulate the retina accordingly. The nanowires give the prosthesis higher resolution than anything achieved by other devices—closer to the dense spacing of photoreceptors in the human retina. The other breakthrough is a wireless device that can transmit power and data to the nanowires over the same wireless link at record speed and energy efficiency.

One of the main differences between the researchers’ prototype and existing retinal prostheses is that the new system does not require a vision sensor outside of the eye to capture a visual scene and then transform it into alternating signals to sequentially stimulate retinal neurons. Instead, the silicon nanowires mimic the retina’s light-sensing cones and rods to directly stimulate retinal cells. Nanowires are bundled into a grid of electrodes, directly activated by light and powered by a single wireless electrical signal. This direct and local translation of incident light into electrical stimulation makes for a much simpler—and scalable—architecture for the prosthesis.

New nano-implant could one day help restore sight
Primary cortical neurons cultured on the surface of an array of optoelectronic nanowires. Here a neuron is pulling the nanowires, indicating the the cell is doing well on this material.  

The power provided to the nanowires from the single wireless electrical signal gives the light-activated electrodes their high sensitivity while also controlling the timing of stimulation.

  “To restore functional vision, it is critical that the neural interface matches the resolution and sensitivity of the ,” said Gert Cauwenberghs, a professor of bioengineering at the Jacobs School of Engineering at UC San Diego and the paper’s senior author.

Wireless telemetry system

Power is delivered wirelessly, from outside the body to the implant, through an inductive powering telemetry system developed by a team led by Cauwenberghs.

The device is highly energy efficient because it minimizes energy losses in wireless power and data transmission and in the stimulation process, recycling electrostatic energy circulating within the inductive resonant tank, and between capacitance on the electrodes and the resonant tank.  Up to 90 percent of the energy transmitted is actually delivered and used for stimulation, which means less RF wireless power emitting radiation in the transmission, and less heating of the surrounding tissue from dissipated power.

The telemetry system is capable of transmitting both power and data over a single pair of inductive coils, one emitting from outside the body, and another on the receiving side in the eye.  The link can send and receive one bit of data for every two cycles of the 13.56 megahertz RF signal; other two-coil systems need at least 5 cycles for every bit transmitted.

New nano-implant could one day help restore sight
Primary cortical neurons cultured on the surface of an array of optoelectronic nanowires. Note the extensive neurite outgrowth and network formation. Credit: University of California – San Diego

Proof-of-concept test

For proof-of-concept, the researchers inserted the wirelessly powered nanowire array beneath a transgenic rat retina with rhodopsin P23H knock-in retinal degeneration. The degenerated retina interfaced in vitro with a microelectrode array for recording extracellular neural action potentials (electrical “spikes” from neural activity).

The horizontal and bipolar neurons fired action potentials preferentially when the prosthesis was exposed to a combination of light and electrical potential—and were silent when either light or electrical bias was absent, confirming the light-activated and voltage-controlled responsivity of the nanowire array.

The wireless device is the result of a collaboration between a multidisciplinary team led by Cauwenberghs, Silva and William R. Freeman, director of the Jacobs Retina Center at UC San Diego, UC San Diego electrical engineering professor Yu-Hwa Lo and Nanovision Biosciences.

A path to clinical translation

Freeman, Silva and Scott Thorogood, have co-founded La Jolla-based Nanovision Biosciences, a partner in this study, to further develop and translate the technology into clinical use, with the goal of restoring functional vision in patients with severe retinal degeneration.  Animal tests with the device are in progress, with clinical trials following.

“We have made rapid progress with the development of the world’s first nanoengineered as a result of the unique partnership we have developed with the team at UC San Diego,” said Thorogood, who is the CEO of Nanovision Biosciences.

CKD: Lower Salt Intake May Reduce Heart Risks.

Posted by

0


A diet with restricted salt intake may help to reduce the risk for cardiovascular disease in patients with chronic kidney disease (CKD), as well as the risk for CKD progression, according to an article published online November 7 in the Journal of the American Society of Nephrology.

Emma J. McMahon, PhD candidate, University of Queensland, Australia, and colleagues conducted a double-blind, placebo-controlled randomized crossover trial involving 20 adult patients with stage 3 to 4 CKD. In the phase I portion of the LowSALT CKD study, the researchers evaluated the effects of high vs low sodium intake on several physiological measures, including ambulatory blood pressure, protein excretion, and body fluid status.

The researchers counseled patients to eat a low-sodium (1080 – 1440 mg/day) diet during the 1-week run-in period of the 6-week study, they then randomly assigned patients to either a high-sodium or low-sodium diet. Those on the high-sodium diet had a goal of 1080 to 1440 mg/day plus 2160 mg/day from a slow-release tablet. Those on the low-sodium diet had a goal of 1080 to 1440 mg/day plus a placebo capsule. Patients crossed over after an intermediate washout week.

The investigators found a mean reduction of 9.7/3.9 mm Hg in blood pressure in patients on the low-salt diet compared with the high-salt diet. The reductions were consistent during a 24-hour period with no significant difference between daytime and nighttime measurements. Researchers also found that patients had reductions in fluid volume, body weight, and protein in the urine while on the low-salt diet.

“If these findings are transferable to the larger CKD population and shown to be sustainable long-term, this could translate to markedly reduced risk of cardiovascular events and progression to end-stage kidney disease, and it could generate considerable health-care savings,” senior author Katrina J. Campbell, PhD, from Princess Alexandra Hospital, Queensland, said in a news release.

“These are clinically significant findings, with this magnitude of blood pressure reduction being comparable to that expected with the addition of an anti-hypertensive medication and larger than effects usually seen with sodium restriction in people without CKD,” McMahon noted in the release. “If maintained long-term, this could reduce risk of progression to end-stage kidney disease — where dialysis or transplant is required to survive — by 30%.”

“This study is salient because few intervention studies have evaluated dietary sodium reduction in patients with CKD, write Cheryl A.M. Anderson, PhD, MPH, and Joachim H. Ix, MD, both from the University of California San Diego School of Medicine, in an accompanying editorial. “The evaluation of other outcomes in addition to BP is an additional strength of the trial.”

Researchers identify key proteins that help establish cell function

Posted by

0


Researchers at the University of California, San Diego School of Medicine have developed a new way to parse and understand how special proteins called “master regulators” read the genome, and consequently turn genes on and off.

Writing in the October 13, 2013 Advance Online Publication of Nature, the scientists say their approach could make it quicker and easier to identify specific gene associated with increased – an essential step toward developing future targeted treatments, preventions and cures for conditions ranging from diabetes to neurodegenerative disease.

“Given the emerging ability to sequence the genomes of individual patients, a major goal is to be able to interpret that DNA sequence with respect to disease risk. What diseases is a person genetically predisposed to?” said principal investigator Christopher Glass, MD, PhD, a professor in the departments of Medicine and Cellular and Molecular Medicine at UC San Diego.

“Mutations that occur in protein-coding regions of the genome are relatively straight forward, but most mutations associated with disease risk actually occur in regions of the genome that do not code for proteins,” said Glass. “A central challenge has been developing a strategy that assesses the potential functional impact of these non-coding mutations. This paper lays the foundation for doing so by examining how natural genetic variation alters the function of genomic regions controlling gene expression in a cell specific-manner.”

Cells use hundreds of different proteins called transcription factors to “read” the genome, employing those instructions to turn genes on and off. These factors tend to be bound close together on the genome, forming functional units called “enhancers.” Glass and colleagues hypothesized that while each cell has tens of thousands of enhancers consisting of myriad combinations of factors, most enhancers are established by just a handful of special transcription factors called “master regulators.” These master regulators play crucial, even disproportional, roles in defining each cell’s identity and function, such as whether it will be a muscle, skin or heart cell.

“Our main idea was that the binding of these master regulators is necessary for the co-binding of the other transcription factors that together enable enhancers to regulate the expression of nearby genes,” Glass said.

The scientists tested and validated their hypothesis by looking at the effects of approximately 4 million DNA sequence differences affecting master regulators in macrophage cells in two strains of mice. Macrophages are a type of immune response cell. They found that DNA sequence mutations deciphered by master regulators not only affected how they bound to the genome, but also impacted neighboring needed to make functional .

The findings have practical importance for scientists and doctors investigating the genetic underpinnings of disease, said Glass. “Without actual knowledge of where the master regulator binds, there is relatively little predictive value of the DNA sequence for non-coding variants. Our work shows that by collecting a focused set of data for the master regulators of a particular cell type, one can greatly reduce the ‘search space’ of the in a particular cell type that would be susceptible to the effects of mutations. This allows prioritization of mutations for subsequent analysis, which can lead to new discoveries and real-world benefits.”

Source:  University of California – San Diego

Researchers Identify Liver Cancer Progenitor Cells Before Tumors Become Visible.

Posted by

0


Stained liver biopsy micrograph showing hepatocellular carcinoma cells with Mallory bodies (reds and blacks).
Stained liver biopsy micrograph showing hepatocellular carcinoma cells with Mallory bodies (reds and blacks).
For the first time, researchers at the University of California, San Diego School of Medicine have isolated and characterized the progenitor cells that eventually give rise to malignant hepatocellular carcinoma (HCC) tumors – the most common form of liver cancer. The researchers found ways to identify and isolate the HCC progenitor cells (HcPC) long before actual tumors were apparent.

<p>Stained liver biopsy micrograph showing hepatocellular carcinoma cells with Mallory bodies (reds and blacks).</p>

Writing in the October 10, 2013 issue of the journal Cell, principal investigator Michael Karin, PhD, Distinguished Professor of Pharmacology and Pathology, and colleagues report that HcPC take form within dysplastic or abnormal lesions often found in damaged or cirrhotic livers. The liver damage can be due to viral infections like hepatitis or from chronic alcohol abuse.

“It was never established whether dysplastic lesions are just a regenerative (healing) response of the liver triggered by tissue damage or are actually pre-malignant lesions that harbor tumor progenitor cells,” said study co-author Debanjan Dhar, PhD, a postdoctoral researcher in Karin’s lab. “Here we show that HcPC are likely derived from dysplastic lesions, can progress to malignant tumors and further demonstrate that the malignant progression of HcPC to full-blown liver cancer depends upon the microenvironment that surrounds them.”

The researchers were able to characterize HcPC based on several biomarkers that distinguish them from normal cells. They also identified cellular signaling pathways activated in HcPC that are critical “to their malignant potential,” said Dhar.

The findings may have profound implications for treating HCC which, while relatively rare in the United States compared to other types of cancer, is difficult to diagnose and treat, with poor prognoses for patients. HCC is usually fatal within three to six months of diagnosis, according to National Institutes of Health data. An estimated 30,000 new cases of liver cancer are diagnosed annually in the U.S., predominantly among men. More than 21,600 Americans die from liver cancer each year, a rate that has been rising slowly for several decades. In other parts of the world, HCC is a major cause of cancer-related deaths.

Most cancers are best detected and treated at the earliest possible stage. HCC is problematic because it develops slowly and frequently displays no symptoms. By the time it is detected, said Dhar, it is usually at an advanced stage with no effective therapy.

“Our findings can be translated into both early detection and therapeutic intervention,” he said. “Better understanding of HcPC cellular networks will provide us with new and effective therapeutic targets.”

For example, the researchers were able to detect “potential” malignant lesions in needle biopsies of a subset of patients infected with the hepatitis C virus, but who hadn’t yet developed HCC. Hepatitis C is a major risk factor for HCC development.

Dhar said identifying premalignant lesions in high-risk patients based on HcPC markers would allow for earlier detection and therapeutic interventions. “Furthermore, in future, therapies can be developed to specifically eliminate the HcPC even before a tumor has developed.”

Co-authors include Guobin He, Joan Font-Burgada, Yuhong Jiang and Shabnam Shalapour, Laboratory of Gene Regulation and Signal Transduction, Departments of Pharmacology and Pathology, UCSD; Hayato Nakagawa, Laboratory of Gene Regulation and Signal Transduction, Departments of Pharmacology and Pathology, UCSD and Department of Gastroenterology, University of Tokyo; Hisanobu Ogata, Laboratory of Gene Regulation and Signal Transduction, Departments of Pharmacology and Pathology, UCSD and Department of Medicine and Clinical Science, Kyushu University, Japan; Ekihiro Seki, Department of Medicine, UCSD; Shawn E. Yost, Bioinformatics Graduate Program and Rady Children’s Hospital-San Diego and Department of Pediatrics, UCSD; Kristen Jepsen, Rady Children’s Hospital-San Diego and Department of Pediatrics, UCSD; Kelly A. Frazer, Rady Children’s Hospital-San Diego and Department of Pediatrics, UCSD, UC San Diego Moores Cancer Center, Clinical and Translational Research Institute, UCSD and Institute for Genomic Medicine, UCSD; Olivier Harismendy, Rady Children’s Hospital-San Diego and Department of Pediatrics, UCSD, UC San Diego Moores Cancer Center, Clinical and Translational Research Institute, UCSD; Maria Hatziapostolou and Dimitrios Iliopoulos, Center for Systems Biomedicine, Geffen School of Medicine, UCLA; Atsushi Suetsugu and Robert M. Hoffman, Department of Surgery, UCSD and Anticancer, Inc., San Diego; and Ryosuke Tateishi  and Kazuhiko Koike, Department of Gastroenterology, University of Tokyo.

Funding support for this research came, in part, from the Superfund Basic Research Program, the National Institutes of Health (CA118165 and CA155120), Wellcome Trust, American Diabetes Association, the Center for Translational Science, the National Center for Research Resources IMAT program, postdoctoral research fellowships from the Damon Runyon Cancer Research Foundation, the American Liver Foundation, Daiichi Sankyo Foundation of Life Science, the California Institute for Regenerative Medicine Stem Cell Training Grant II, Kanzawa Medical Research Foundation, the German Research Foundation and a Young Investigator Award from the National Childhood Cancer Foundation “CureSearch.”

<p>Stained liver biopsy micrograph showing hepatocellular carcinoma cells with Mallory bodies (reds and blacks).</p>
Stained liver biopsy micrograph showing hepatocellular carcinoma cells with Mallory bodies (reds and blacks).
For the first time, researchers at the University of California, San Diego School of Medicine have isolated and characterized the progenitor cells that eventually give rise to malignant hepatocellular carcinoma (HCC) tumors – the most common form of liver cancer. The researchers found ways to identify and isolate the HCC progenitor cells (HcPC) long before actual tumors were apparent.

Writing in the October 10, 2013 issue of the journal Cell, principal investigator Michael Karin, PhD, Distinguished Professor of Pharmacology and Pathology, and colleagues report that HcPC take form within dysplastic or abnormal lesions often found in damaged or cirrhotic livers. The liver damage can be due to viral infections like hepatitis or from chronic alcohol abuse.

“It was never established whether dysplastic lesions are just a regenerative (healing) response of the liver triggered by tissue damage or are actually pre-malignant lesions that harbor tumor progenitor cells,” said study co-author Debanjan Dhar, PhD, a postdoctoral researcher in Karin’s lab. “Here we show that HcPC are likely derived from dysplastic lesions, can progress to malignant tumors and further demonstrate that the malignant progression of HcPC to full-blown liver cancer depends upon the microenvironment that surrounds them.”

The researchers were able to characterize HcPC based on several biomarkers that distinguish them from normal cells. They also identified cellular signaling pathways activated in HcPC that are critical “to their malignant potential,” said Dhar.

The findings may have profound implications for treating HCC which, while relatively rare in the United States compared to other types of cancer, is difficult to diagnose and treat, with poor prognoses for patients. HCC is usually fatal within three to six months of diagnosis, according to National Institutes of Health data. An estimated 30,000 new cases of liver cancer are diagnosed annually in the U.S., predominantly among men. More than 21,600 Americans die from liver cancer each year, a rate that has been rising slowly for several decades. In other parts of the world, HCC is a major cause of cancer-related deaths.

Most cancers are best detected and treated at the earliest possible stage. HCC is problematic because it develops slowly and frequently displays no symptoms. By the time it is detected, said Dhar, it is usually at an advanced stage with no effective therapy.

“Our findings can be translated into both early detection and therapeutic intervention,” he said. “Better understanding of HcPC cellular networks will provide us with new and effective therapeutic targets.”

For example, the researchers were able to detect “potential” malignant lesions in needle biopsies of a subset of patients infected with the hepatitis C virus, but who hadn’t yet developed HCC. Hepatitis C is a major risk factor for HCC development.

Dhar said identifying premalignant lesions in high-risk patients based on HcPC markers would allow for earlier detection and therapeutic interventions. “Furthermore, in future, therapies can be developed to specifically eliminate the HcPC even before a tumor has developed.”

Co-authors include Guobin He, Joan Font-Burgada, Yuhong Jiang and Shabnam Shalapour, Laboratory of Gene Regulation and Signal Transduction, Departments of Pharmacology and Pathology, UCSD; Hayato Nakagawa, Laboratory of Gene Regulation and Signal Transduction, Departments of Pharmacology and Pathology, UCSD and Department of Gastroenterology, University of Tokyo; Hisanobu Ogata, Laboratory of Gene Regulation and Signal Transduction, Departments of Pharmacology and Pathology, UCSD and Department of Medicine and Clinical Science, Kyushu University, Japan; Ekihiro Seki, Department of Medicine, UCSD; Shawn E. Yost, Bioinformatics Graduate Program and Rady Children’s Hospital-San Diego and Department of Pediatrics, UCSD; Kristen Jepsen, Rady Children’s Hospital-San Diego and Department of Pediatrics, UCSD; Kelly A. Frazer, Rady Children’s Hospital-San Diego and Department of Pediatrics, UCSD, UC San Diego Moores Cancer Center, Clinical and Translational Research Institute, UCSD and Institute for Genomic Medicine, UCSD; Olivier Harismendy, Rady Children’s Hospital-San Diego and Department of Pediatrics, UCSD, UC San Diego Moores Cancer Center, Clinical and Translational Research Institute, UCSD; Maria Hatziapostolou and Dimitrios Iliopoulos, Center for Systems Biomedicine, Geffen School of Medicine, UCLA; Atsushi Suetsugu and Robert M. Hoffman, Department of Surgery, UCSD and Anticancer, Inc., San Diego; and Ryosuke Tateishi  and Kazuhiko Koike, Department of Gastroenterology, University of Tokyo.

Funding support for this research came, in part, from the Superfund Basic Research Program, the National Institutes of Health (CA118165 and CA155120), Wellcome Trust, American Diabetes Association, the Center for Translational Science, the National Center for Research Resources IMAT program, postdoctoral research fellowships from the Damon Runyon Cancer Research Foundation, the American Liver Foundation, Daiichi Sankyo Foundation of Life Science, the California Institute for Regenerative Medicine Stem Cell Training Grant II, Kanzawa Medical Research Foundation, the German Research Foundation and a Young Investigator Award from the National Childhood Cancer Foundation “CureSearch.”

Contact lenses bestow telescopic vision.

Posted by

0


Researchers have created contact lenses which, when paired with special spectacles, bestow telescopic vision on their wearers.

lens _68497754_lens

The contact-lens-and-spectacles combination magnifies scene details by 2.8 times.

lens

Polarising filters in the spectacles allow wearers to switch between normal and telescopic vision.

The telescopic sight system has been developed to help people suffering age-related blindness.

Age-related macular degeneration is one of the most common forms of blindness and damages the part of the eye, the macula, that handles fine detail. As this area degenerates, sufferers lose the ability to recognise faces and perform tasks, such as driving and reading, that rely on picking up details.

Precise control

The contact lens created by the researchers has a central region that lets light through for normal vision. The telescopic element sits in a ring around this central region. Tiny aluminium mirrors scored with a specific pattern act as a magnifier as they bounce the light around four times within the ring before directing it towards the retina.

In ordinary use, the magnified image is not seen as it is blocked by polarising filters set in a companion pair of spectacles. Wearers can switch it on by changing the filters on the spectacles so the only light falling on their retina comes from the magnified stream.

For their filtering system, the researchers, led by Joseph Ford at UC San Diego and Eric Tremblay at Switzerland’s EPFL, adapted a pair of glasses that Samsung produces for some of its 3D TV sets. In normal use, these spectacles create a 3D effect by alternately blocking the right or left lens.

The prototype contact lens produced by the team is 8mm in diameter, 1mm thick at its centre and 1.17mm thick in its magnifying ring.

“The most difficult part of the project was making the lens breathable,” Dr Tremblay told the BBC. “If you want to wear the lens for more than 30 minutes you need to make it breathable.”

Gases have to be able to penetrate the lens to keep the parts of the eye covered by the contact, especially the cornea, supplied with oxygen, he said.

The team has solved this problem by producing lenses riddled with tiny channels that let oxygen flow through.

However, said Dr Tremblay, this made manufacturing the lenses much more difficult.

“The fabrication tolerances are quite challenging because everything has to be so precise,” he said.

Despite this, gas-permeable versions of the telescopic lens are being prepared that will be used in clinical trials in November, he said. Eventually it should be possible for those with age-related sight problems to wear the telescopic lenses all day.

The lenses are an improvement on other ways these sight problems have been tackled which has included surgery to implant a telescopic lens or wearing bulky spectacles that have telescopic lenses forming part of the main lens.

Clara Eaglen, eye health campaigns manager at the RNIB said the research looked “interesting” and praised its focus on macular degeneration.

“It is encouraging that innovative products such as these telescopic contact lenses are being developed, especially as they aim to make the most of a person’s existing vision,” she said. “”Anything that helps to maximise functioning vision is very important as this helps people with sight loss to regain some independence and get out and about again, helping to reduce isolation.”

The lenses may one day find their way into other areas as the research was being funded by Darpa, the research arm of the US military.

“They are not so concerned about macular degeneration,” he said. “They are concerned with super vision which is a much harder problem.

“That’s because the standard is much higher if you are trying to improve vision rather than helping someone whose eyesight has deteriorated,” he said.

Source: BBC

 

Metal Oxide Chips Show Promise as Transistors.

Posted by

0


metal-oxide-chips-show-promise-as-transistors_1

Materials that flip from insulator to conductor could make more energy-efficient transistors, although the metals are not yet close to competing with silicon

The switches in most electronic circuits are made of silicon, one of the commonest elements. But their successors might contain materials that, for now, are lab-grown oddities: strongly correlated metal oxides.

The allure of these materials lies in the outer shells of electrons surrounding their metal atoms. The shells are incomplete, leaving the electrons free to participate in coordinated quantum-mechanical behavior. In some materials, electrons pair up to produce super­conductivity, or coordinate their spins to produce magnetism. Other materials can switch from being an insulator to a conductor.

Unlike transitions to superconductivity, which happen as temperatures approach absolute zero, the insulating-to-conducting transition typically happens as temperature increases, and sometimes occurs near room temperature. That has raised hopes that metal oxides could be used instead of silicon to make transistors. A spate of results is now making that look feasible. “People are interested in seeing if oxides can make it to applications,” says Manuel Bibes, a physicist at the Joint Physics Unit in Palaiseau, France, which is run by the French National Research Center and electronics company Thales.

Metal oxide transistors have the potential to consume less power than silicon switches, because the phase transition frees electrons from their localized state near each atom, without moving them through the bulk material. By contrast, silicon switches work by pulling electrons through the material to a channel where they conduct current (see ‘Go with the flow’).

In the past 5–10 years, researchers have succeeded in growing high-quality thin films of the metal oxides — overcoming one of the major barriers to applications. In July 2012, for example, a group in Japan reported that it had deposited a thin film of vanadium dioxide that underwent a phase transition in response to an applied electric field — proof that the material could be used as an electronic switch.

And last month, a group led by Shriram Ramanathan, a materials scientist at Harvard University in Cambridge, Massachusetts, addressed a fabrication challenge by growing a thin film of samarium nickelate on top of a substrate made of silicon and silicon dioxide.

The nickelate was deposited at a relatively low temperature that did not disturb the underlying silicon layers, raising the possibility of manufacturing metal oxides on top of silicon wafers to form three-dimensional chips, says Andrew Millis, a solid-state theorist at Columbia University in New York. Not only would that allow computing power to be packed much more densely, says Millis, but it would also permit metal oxide switches to be built on top of existing circuit architectures.

Other groups are trying to understand the nature of the phase transition. In January, Ivan Schuller, a solid-state physicist at the University of California, San Diego, and his colleagues showed that in vanadium oxide, the transition is in large part caused by micrometer-scale heating by the applied electric field.

Some point to Schuller’s work as evidence that metal oxides will never make fast switches, because heating effects are usually quite slow. But Ramanathan says that his own measurements on vanadium oxide demonstrate that the phase transition is quite fast — less than a few nanoseconds — and that it should not hinder applications.

Some physicists are finding further examples of potentially useful materials. Bernhard Keimer at the Max Planck Institute for Solid State Research in Stuttgart, Germany, alternates thin layers of metal oxides to form composites that often turn out to have serendipitous properties. His group layered conducting lanthanum nickelate and insulating lanthanum aluminate and found that the composite underwent a transition between the two properties.

The highest phase-transition temperature for the composite was 150 kelvin above absolute zero — too low for practical applications. But the group is now trying to replicate the phenomenon in other materials that might have higher transition temperatures.

Sandip Tiwari, an applied physicist at Cornell University in Ithaca, New York, acknowledges that metal oxides are not yet close to competing with silicon. But given recent progress, he feels that researchers need to start trying to implement them in devices. That way, he says, all the properties needed for a good transistor will be developed in tandem. “If you just look at whatever property is your favorite, you won’t get them all.”

Source: Scientific American.

Stronger statins associated with muscle problems.

Posted by

0


Among patients taking statins, those who reported experiencing muscle problems were prescribed a stronger or more potent statin, according to study results recently published in PLoS One.

Researchers analyzed 147,789 case reports from the FDA Adverse Event Reporting System (AERS) database linking muscle-related adverse events to statin use from July 2005 to March 2011. Statins selected for analysis included: atorvastatin (Lipitor, Pfizer), simvastatin (Zocor, Merck), lovastatin (Mevacor, Merck), pravastatin (Pravachol, Bristol-Myers Squibb), rosuvastatin (Crestor, AstraZeneca), fluvastatin (Lescol, Novartis) and generic equivalents and foreign designations. Death, disability and hospitalization were collected as outcome measures for the main adverse event categories, which included joints and tendons, muscle atrophy and injury, and muscle coordination and weakness.

Overall, researchers found that relative risk rates were consistently higher for rosuvastatin and fluvastatin, intermediate for atorvastatin and simvastatin and low for pravastatin and lovastatin. When all muscle categories were incorporated, study results showed that rosuvastatin had the highest ranked risk, followed by atorvastatin (55%), simvastatin (26%), pravastatin (17%) and lovastatin (7.5%).

“These findings underscore that stronger statins bear higher risk — and should be used with greater caution and circumspection,” Beatrice Golomb, MD, PhD, professor in the departments of medicine and family and preventative medicine at the University of California, San Diego, said in a press release. “These rankings closely match the individual potencies of each statin. Thus, the strength of the statin drug appears to be a dominant factor in determining how likely muscle problems are to occur.”

Source: Endocrine Today.