Pancreatic cancer 's high death rate is partly blamed on the difficulty of early detection. Teenage scientist Jack Andraka has come up with a cheap and simple way to test for it.
Pancreatic cancer is a killer – and one that is very hard to detect. One of the reasons its survival rate is so poor that it has few symptoms in the early stages.
Partly spurred by the death of his uncle, 16-year-old scientist and researcher Jack Andraka vowed to find a quick and cheap way to test for signs of the disease.
Andraka's research – incuding writing to 200 science professors – led to him developing a dipstick diagnostic test which searches for a biomarker for pancreatic cancer. It can also be used to test for lung and ovarian cancer.
He tells BBC Future about his quest.
Source: http://www.bbc.com/future/story/20130701-perfecting-early-cancer-detection
Innovative news from the world of technology. Objective is to keep a history of interesting new technology and see if it came to fruition.
Wednesday, July 31, 2013
Tuesday, July 23, 2013
Tuesday, July 16, 2013
Better diagnosis and treatment of cancer
Novel quantum dot-based technique sees 100 different molecules in a single cell.
Better diagnosis and treatment of cancer could hinge on the ability to rapidly map out networks of dozens of molecules in individual tumor cells.
New research from the University of Washington offers a more comprehensive way of analyzing a single cell’s unique behavior and could reveal patterns that indicate why a cell will or will not become malignant.
Xiaohu Gua and graduate student Pavel Zrazhevskiy have used an array of distinctly colored quantum dots to illuminate 100 biomarkers, a ten-fold increase from the current research standard, to help analyze individual cells from cultures or tissue biopsies.
Other approaches have measured multiple biomarkers in a single cell, but what makes this technique promising is that it reuses the same precious tissue sample in a cyclical process to measure 100 biomolecules in groups of ten.
The investigators then inject a solution of ten of these antibody-quantum dot pairs onto a tissue sample and use a fluorescence microscope to quantify which of the constructs bind at the single cell level.
Once the measurement is complete, they then wash the tissue sample with a fluid of detergents at low pH to get rid of the antibodies and quantum dots without degrading the tissue sample, and repeat the staining step for different target molecules
The two investigators have shown that they can repeat this process at least ten times without producing any signs of tissue damage.
The researchers note that because this methodology uses commercially available enzymes and standard fluorescence microscopes, it is relatively low cost. They also plan to automate the procedure using microfluidics and automated image processing technologies.
This work, which was supported in part by the National Cancer Institute, is detailed in an open access paper in Nature Communications.
Pavel Zrazhevskiy, Xiaohu Gao, Quantum dot imaging platform for single-cell molecular profiling, Nature Communications, 2013, DOI: 10.1038/ncomms2635 (open access)
Source: http://www.kurzweilai.net/novel-quantum-dot-based-technique-sees-100-different-molecules-in-a-single-cell
Better diagnosis and treatment of cancer could hinge on the ability to rapidly map out networks of dozens of molecules in individual tumor cells.
New research from the University of Washington offers a more comprehensive way of analyzing a single cell’s unique behavior and could reveal patterns that indicate why a cell will or will not become malignant.
Xiaohu Gua and graduate student Pavel Zrazhevskiy have used an array of distinctly colored quantum dots to illuminate 100 biomarkers, a ten-fold increase from the current research standard, to help analyze individual cells from cultures or tissue biopsies.
Other approaches have measured multiple biomarkers in a single cell, but what makes this technique promising is that it reuses the same precious tissue sample in a cyclical process to measure 100 biomolecules in groups of ten.
The investigators then inject a solution of ten of these antibody-quantum dot pairs onto a tissue sample and use a fluorescence microscope to quantify which of the constructs bind at the single cell level.
Once the measurement is complete, they then wash the tissue sample with a fluid of detergents at low pH to get rid of the antibodies and quantum dots without degrading the tissue sample, and repeat the staining step for different target molecules
The two investigators have shown that they can repeat this process at least ten times without producing any signs of tissue damage.
The researchers note that because this methodology uses commercially available enzymes and standard fluorescence microscopes, it is relatively low cost. They also plan to automate the procedure using microfluidics and automated image processing technologies.
This work, which was supported in part by the National Cancer Institute, is detailed in an open access paper in Nature Communications.
Pavel Zrazhevskiy, Xiaohu Gao, Quantum dot imaging platform for single-cell molecular profiling, Nature Communications, 2013, DOI: 10.1038/ncomms2635 (open access)
Source: http://www.kurzweilai.net/novel-quantum-dot-based-technique-sees-100-different-molecules-in-a-single-cell
New theory uncovers cancer’s deep evolutionary roots
Authors predict that if cancer cells are saturated with oxygen but deprived of sugar, it will slow them down or even even kill them.
A new way to look at cancer — by tracing its deep evolutionary roots to the dawn of multicellularity more than a billion years ago — has been proposed by Paul Davies of Arizona State University’s Beyond Center for Fundamental Concepts in Science in collaboration with Charles Lineweaver of the Australian National University.
Their view of cancer is outlined in the article “Exposing cancer’s deep evolutionary roots,” written by Davies (available free with registration). It appears in a special July issue of Physics World devoted to the physics of cancer.
The new theory predicts that as cancer progresses through more and more malignant stages, it will express genes that are more deeply conserved among multicellular organisms, and so are in some sense more ancient. Davies and Lineweaver are currently testing this prediction by comparing gene expression data from cancer biopsies with phylogenetic trees going back 1.6 billion years, with the help of Luis Cisneros, a postdoctoral researcher with ASU’s Beyond Center.
“It is clear that some radically new thinking is needed,” Davies states. “Like aging, cancer seems to be a deeply embedded part of the life process. Also like aging, cancer generally cannot be cured but its effects can certainly be mitigated, for example, by delaying onset and extending periods of dormancy. But we will learn to do this effectively only when we better understand cancer, including its place in the great sweep of evolutionary history.”
Paul Davies, Exposing cancer's deep evolutionary roots, Physics World, 2013 (requires free registration)
Source: http://www.kurzweilai.net/new-theory-uncovers-cancers-deep-evolutionary-roots
A new way to look at cancer — by tracing its deep evolutionary roots to the dawn of multicellularity more than a billion years ago — has been proposed by Paul Davies of Arizona State University’s Beyond Center for Fundamental Concepts in Science in collaboration with Charles Lineweaver of the Australian National University.
Their view of cancer is outlined in the article “Exposing cancer’s deep evolutionary roots,” written by Davies (available free with registration). It appears in a special July issue of Physics World devoted to the physics of cancer.
The new theory predicts that as cancer progresses through more and more malignant stages, it will express genes that are more deeply conserved among multicellular organisms, and so are in some sense more ancient. Davies and Lineweaver are currently testing this prediction by comparing gene expression data from cancer biopsies with phylogenetic trees going back 1.6 billion years, with the help of Luis Cisneros, a postdoctoral researcher with ASU’s Beyond Center.
“It is clear that some radically new thinking is needed,” Davies states. “Like aging, cancer seems to be a deeply embedded part of the life process. Also like aging, cancer generally cannot be cured but its effects can certainly be mitigated, for example, by delaying onset and extending periods of dormancy. But we will learn to do this effectively only when we better understand cancer, including its place in the great sweep of evolutionary history.”
Paul Davies, Exposing cancer's deep evolutionary roots, Physics World, 2013 (requires free registration)
Source: http://www.kurzweilai.net/new-theory-uncovers-cancers-deep-evolutionary-roots
Tuesday, July 09, 2013
Scientists Tailor Make Anti-Cancer Agent
Scientists at the Walter and Eliza Hall Institute in Australia and their collaborators have tailor-made a new chemical compound that blocks a key cancer protein. The development of the compound, called WEHI-539, is an important step towards the design of a potential new anti-cancer agent.
The researchers designed the compound WEHI-539 to bind and block the function of a protein called BCL-XL that normally prevents cells from dying. BCL-XL has been linked to poor responses to treatment in cancer patients.
The death and elimination of abnormal cells in the body is an important safeguard against cancer development. But cancer cells often acquire genetic changes that allow them to escape cell death, which also reduces the effectiveness of anti-cancer treatments such as chemotherapy.
Cancer cells can become long-lived by producing high levels of BCL-XL protein, and high levels of BCL-XL are also associated with poorer outcomes for patients with lung, stomach, colon and pancreatic cancer.
Dr. Guillaume Lessene, who led the research team in collaboration with Genentech, said the development of WEHI-539 was an important milestone on the way to creating potential anti-cancer agents that act to restore cell death by inhibiting BCL-XL.
Publishing in the journal Nature Chemical Biology, Dr. Lessene said WEHI-539 was the product of a sustained research program. Article link: Lessene et al. (2013) Structure-guided design of a selective BCL-XL inhibitor
Source: http://www.asianscientist.com/health-medicine/scientists-tailor-anti-cancer-agent-2013/
The researchers designed the compound WEHI-539 to bind and block the function of a protein called BCL-XL that normally prevents cells from dying. BCL-XL has been linked to poor responses to treatment in cancer patients.
The death and elimination of abnormal cells in the body is an important safeguard against cancer development. But cancer cells often acquire genetic changes that allow them to escape cell death, which also reduces the effectiveness of anti-cancer treatments such as chemotherapy.
Cancer cells can become long-lived by producing high levels of BCL-XL protein, and high levels of BCL-XL are also associated with poorer outcomes for patients with lung, stomach, colon and pancreatic cancer.
Dr. Guillaume Lessene, who led the research team in collaboration with Genentech, said the development of WEHI-539 was an important milestone on the way to creating potential anti-cancer agents that act to restore cell death by inhibiting BCL-XL.
Publishing in the journal Nature Chemical Biology, Dr. Lessene said WEHI-539 was the product of a sustained research program. Article link: Lessene et al. (2013) Structure-guided design of a selective BCL-XL inhibitor
Source: http://www.asianscientist.com/health-medicine/scientists-tailor-anti-cancer-agent-2013/
Thursday, June 20, 2013
High-molecular-mass hyaluronan mediates the cancer resistance of thenaked mole rat
Xiao Tian Jorge Azpurua Christopher HineAmita Vaidya Max Myakishev-Rempel Julia Ablaeva Zhiyong Mao Eviatar Nevo Vera Gorbunova Andrei Seluanov
The naked mole rat (Heterocephalus glaber) displays exceptional longevity, with a maximum lifespan exceeding 30 years1, 2, 3. This is the longest reported lifespan for a rodent species and is especially striking considering the small body mass of the naked mole rat. In comparison, a similarly sized house mouse has a maximum lifespan of 4 years4, 5. In addition to their longevity, naked mole rats show an unusual resistance to cancer.
We speculate that naked mole rats have evolved a higher concentration of HA in the skin to provide skin elasticity needed for life in underground tunnels. This trait may have then been co-opted to provide cancer resistance and longevity to this species.
Source: http://www.nature.com/nature/journal/vaop/ncurrent/full/nature12234.html#auth-1
Friday, May 31, 2013
Vehicle-to-grid (V2G) system
Vehicle-to-grid (V2G) describes a system in which plug-in electric vehicles, such as electric cars (BEVs) and plug-in hybrids (PHEVs), communicate with the power grid to sell demand response services by either delivering electricity into the grid or by throttling their charging rate.[1][2]
Vehicle-to-grid can be used with such gridable vehicles, that is, plug-in electric vehicles (BEVs and PHEVs), with grid capacity. Since most vehicles are parked an average of 95 percent of the time, their batteries could be used to let electricity flow from the car to the power lines and back, with a value to the utilities of up to $4,000 per year per car.
BMW, Continental, Daimler, Fraunhofer, RWE, Siemens, TU Dortmund and VW – the partners in the new research project “eNterop” belong to the German industrial and research scene’s elite. They are now working with domestic proponents of international standardization of “vehicle-to-grid communication” (V2G) for electric vehicle networks on the next stage: an open test platform for the interface between electric vehicles and charging infrastructures. Their goal is the rapid establishment of standards for supply and communications systems between vehicles and electric power grids.
Electric vehicles will have to be able to communicate with grids reliably and charge or supply electricity at charging stations regardless of their make.
Sources:
http://www.iff.fraunhofer.de/en/press/press-releases/2013/electric-vehicles-network-standard.html
http://en.wikipedia.org/wiki/Vehicle-to-grid
Vehicle-to-grid can be used with such gridable vehicles, that is, plug-in electric vehicles (BEVs and PHEVs), with grid capacity. Since most vehicles are parked an average of 95 percent of the time, their batteries could be used to let electricity flow from the car to the power lines and back, with a value to the utilities of up to $4,000 per year per car.
BMW, Continental, Daimler, Fraunhofer, RWE, Siemens, TU Dortmund and VW – the partners in the new research project “eNterop” belong to the German industrial and research scene’s elite. They are now working with domestic proponents of international standardization of “vehicle-to-grid communication” (V2G) for electric vehicle networks on the next stage: an open test platform for the interface between electric vehicles and charging infrastructures. Their goal is the rapid establishment of standards for supply and communications systems between vehicles and electric power grids.
Electric vehicles will have to be able to communicate with grids reliably and charge or supply electricity at charging stations regardless of their make.
Sources:
http://www.iff.fraunhofer.de/en/press/press-releases/2013/electric-vehicles-network-standard.html
http://en.wikipedia.org/wiki/Vehicle-to-grid
Monday, May 27, 2013
Can we detect cancer earlier?
Silicon Valley research lab found a way to identify cancer cells in a drop of blood.
Source: http://thenextweb.com/insider/2013/05/19/what-the-future-looks-like-inside-the-lab-that-brought-us-siri-the-mouse-and-the-internet-itself/
Related links: http://www.kurzweilai.net/how-to-detect-microvesicles-in-the-bloodstream-to-diagnose-and-monitor-brain-cancer
Source: http://thenextweb.com/insider/2013/05/19/what-the-future-looks-like-inside-the-lab-that-brought-us-siri-the-mouse-and-the-internet-itself/
Related links: http://www.kurzweilai.net/how-to-detect-microvesicles-in-the-bloodstream-to-diagnose-and-monitor-brain-cancer
Friday, May 24, 2013
Cancer cell enzymes shown to act as 'good cops'
Enzymes released by cancerous cells have a protective function and are not one of the "bad guys", say researchers from the University of East Anglia.
Their study found the MMP-8 enzyme sent a signal to the immune system to attack the tumour.
Scientists from UEA worked with clinicians at the Norfolk and Norwich University Hospital to look in detail at the patterns of MMPs in breast tumours from patients.
Their study, published in the Journal of Biological Chemistry, reveals that the matrix metalloproteinase-8 enzyme (MMP-8) could be acting as the 'good guy' by alerting the immune system to the location of the tumour.
"They were once thought to act like 'molecular scissors' to snip away at the scaffolding structures outside cells and clear a path for the cancer cells to invade and spread to other organs.
"However, breast tumour cells that over-produce MMP-8 don't survive long-term - the enzyme stops them growing," he said.
"We now think that in tumours, MMP-8 acts as a sort of 'find me' signal to the immune system, which then becomes activated to attack the tumour, which may help to explain its protective function."
Dr Emma Smith, senior science information officer at Cancer Research UK, said: "This study provides very early clues as to how the MMP-8 protein might actually play the role of a 'good cop' and recruit immune cells to fight breast cancer.
"But these are early findings from cells grown in a lab, and more research is needed to see if the molecules found by the scientists alert immune cells to cancers in women."
Source: http://www.bbc.co.uk/news/health-22645780#
Their study found the MMP-8 enzyme sent a signal to the immune system to attack the tumour.
Scientists from UEA worked with clinicians at the Norfolk and Norwich University Hospital to look in detail at the patterns of MMPs in breast tumours from patients.
Their study, published in the Journal of Biological Chemistry, reveals that the matrix metalloproteinase-8 enzyme (MMP-8) could be acting as the 'good guy' by alerting the immune system to the location of the tumour.
"They were once thought to act like 'molecular scissors' to snip away at the scaffolding structures outside cells and clear a path for the cancer cells to invade and spread to other organs.
"However, breast tumour cells that over-produce MMP-8 don't survive long-term - the enzyme stops them growing," he said.
"We now think that in tumours, MMP-8 acts as a sort of 'find me' signal to the immune system, which then becomes activated to attack the tumour, which may help to explain its protective function."
Dr Emma Smith, senior science information officer at Cancer Research UK, said: "This study provides very early clues as to how the MMP-8 protein might actually play the role of a 'good cop' and recruit immune cells to fight breast cancer.
"But these are early findings from cells grown in a lab, and more research is needed to see if the molecules found by the scientists alert immune cells to cancers in women."
Source: http://www.bbc.co.uk/news/health-22645780#
Quantum-dot solar cells have great potential for solar cells
There has been great interest in recent years in using tiny particles called quantum dots to produce low-cost, easily manufactured, stable photovoltaic cells.
Now, for the most widely used type of quantum dots, made of compounds called metal chalcogenides, researchers from MIT may have found the key: The limiting factor seems to be off-kilter ratios of the two basic components that make up the dots.
There has been “a lot of excitement” about the potential for quantum dots in applications including electronic devices, lighting and solar cells, Grossman says. Among other potential advantages, quantum-dot solar cells could be made in a low-temperature process, by depositing material from a solution at room temperature, rather than the high-temperature, energy-intensive processes used for conventional photovoltaics. In addition, such devices could be precisely “tuned,” to obtain maximum conversion of specific wavelengths (colors) of light to energy, by adjusting the size and shape of the particles.
To go beyond the efficiencies achieved so far with quantum-dot solar cells, Grossman says, researchers needed to understand why the charges got trapped in the material. “We found something quite different than what people thought was causing the problem,” he says.
Giulia Galli, a professor of physics and chemistry at the University of California at Davis who was not connected with this research, says it is “quite a creative and important piece of work,” and adds that, “I'm pretty sure this will stimulate new experiments” to engineer the stoichiometry of quantum dots in order to control their properties.
In addition to Kim and Grossman, the work was carried out by former MIT postdoc Joo-Hyoung Lee, now at the Gwangju Institute of Science and Technology in South Korea, and Dong-Ho Kim of the Samsung Advanced Institute of Technology (SAIT) in Cambridge, Mass. The work was supported by SAIT, and is part of a larger quantum-dot solar cell program within the SAIT-MIT alliance that includes professors Vladimir Bulovic and Moungi Bawendi.
Source: http://web.mit.edu/newsoffice/2013/balance-key-to-making-quantum-dot-solar-cells-work-0524.html
Now, for the most widely used type of quantum dots, made of compounds called metal chalcogenides, researchers from MIT may have found the key: The limiting factor seems to be off-kilter ratios of the two basic components that make up the dots.
The new findings — by Jeffrey Grossman, the Carl Richard Soderberg Associate Professor of Power Engineering, materials science and engineering graduate student Donghun Kim, and two other researchers — were reported this month in the journal Physical Review Letters.
To go beyond the efficiencies achieved so far with quantum-dot solar cells, Grossman says, researchers needed to understand why the charges got trapped in the material. “We found something quite different than what people thought was causing the problem,” he says.
Giulia Galli, a professor of physics and chemistry at the University of California at Davis who was not connected with this research, says it is “quite a creative and important piece of work,” and adds that, “I'm pretty sure this will stimulate new experiments” to engineer the stoichiometry of quantum dots in order to control their properties.
In addition to Kim and Grossman, the work was carried out by former MIT postdoc Joo-Hyoung Lee, now at the Gwangju Institute of Science and Technology in South Korea, and Dong-Ho Kim of the Samsung Advanced Institute of Technology (SAIT) in Cambridge, Mass. The work was supported by SAIT, and is part of a larger quantum-dot solar cell program within the SAIT-MIT alliance that includes professors Vladimir Bulovic and Moungi Bawendi.
Source: http://web.mit.edu/newsoffice/2013/balance-key-to-making-quantum-dot-solar-cells-work-0524.html
Tuesday, May 21, 2013
Cancer risk gene testing announced
A pioneering programme to test cancer patients for nearly 100 risk genes is to start in London and could represent the future of treatment in the NHS.
It will look for genes such as those which led Hollywood actress Angelina Jolie to have a double mastectomy.
The results will be used to pick targeted drugs or decide how much of the tissue around a tumour to remove.
It will also highlight patients at high risk of additional cancers, who need to be monitored closely.
Some people with BRCA gene mutations have an 80% risk of breast cancer.
The testing will be run by the Institute of Cancer Research and The Royal Marsden hospital in London.
Prof Nazneen Rahman, lead investigator of the programme said: "It is very important to know if a mutation in a person's genetic blueprint has caused their cancer.
Prof Martin Gore, the medical director of the Royal Marsden, said this would be "an exciting change of practice", which patients were ready for. "Patient's want to know. I'm asked several times a day, 'Is this hereditary?' There's no point pretending that patients don't want to know."
The test, developed by biotechnology firm Illumina, looks for 97 genes which increase the risk of cancer. More risk genes can be added to the test once they are discovered.
It is available for use in other hospitals, but the researchers say this is the first attempt at introducing mass cancer-risk gene testing as a cornerstone of treatment.
Prof Peter Johnson, Cancer Research UK's chief clinician, said: "Researchers now have a wealth of information about the inherited gene faults that increase a person's cancer risk, and this knowledge can help tailor treatments for patients whose cancers are linked to these mutations.
Dr Caitlin Palframan, from Breakthrough Breast Cancer, said: "This programme has a lot of potential as this type of testing may help lay the ground for more personalised treatment for people with breast cancer.
Source: http://www.bbc.co.uk/news/health-22599402#
It will look for genes such as those which led Hollywood actress Angelina Jolie to have a double mastectomy.
The results will be used to pick targeted drugs or decide how much of the tissue around a tumour to remove.
It will also highlight patients at high risk of additional cancers, who need to be monitored closely.
Some people with BRCA gene mutations have an 80% risk of breast cancer.
The testing will be run by the Institute of Cancer Research and The Royal Marsden hospital in London.
Prof Nazneen Rahman, lead investigator of the programme said: "It is very important to know if a mutation in a person's genetic blueprint has caused their cancer.
Prof Martin Gore, the medical director of the Royal Marsden, said this would be "an exciting change of practice", which patients were ready for. "Patient's want to know. I'm asked several times a day, 'Is this hereditary?' There's no point pretending that patients don't want to know."
The test, developed by biotechnology firm Illumina, looks for 97 genes which increase the risk of cancer. More risk genes can be added to the test once they are discovered.
It is available for use in other hospitals, but the researchers say this is the first attempt at introducing mass cancer-risk gene testing as a cornerstone of treatment.
Prof Peter Johnson, Cancer Research UK's chief clinician, said: "Researchers now have a wealth of information about the inherited gene faults that increase a person's cancer risk, and this knowledge can help tailor treatments for patients whose cancers are linked to these mutations.
Dr Caitlin Palframan, from Breakthrough Breast Cancer, said: "This programme has a lot of potential as this type of testing may help lay the ground for more personalised treatment for people with breast cancer.
Source: http://www.bbc.co.uk/news/health-22599402#
Wednesday, May 15, 2013
Next generation of military drones
The next generation of military drones are here, and they're controlled by algorithms and designed for sea combat. On May 14, the U.S. Navy successfully launched the experimental X-47B Unmanned Combat Air System from the USS George H.W. Bush and landed the drone at a naval air base in Maryland. When complete, the X-47B will be able to both take off and land on the same aircraft carrier.
But unlike conventional UAVs, there's something different about the X-47B. The X-47B isn't only unmanned... it's autonomous, too. The drone is descended from DARPA's Joint Unmanned Combat Air Systems (J-UCAS) program, which created UAV control systems that depend entirely on algorithms, sensors, and computer code. Although the X-47B still requires occasional human input, it operates mostly autonomously along pre-programmed flight routes. Humans only override the X-47B's programming if anomalies happen.
Source: http://www.fastcompany.com/3009724/inside-the-navys-historic-embrace-of-at-sea-combat-drones
But unlike conventional UAVs, there's something different about the X-47B. The X-47B isn't only unmanned... it's autonomous, too. The drone is descended from DARPA's Joint Unmanned Combat Air Systems (J-UCAS) program, which created UAV control systems that depend entirely on algorithms, sensors, and computer code. Although the X-47B still requires occasional human input, it operates mostly autonomously along pre-programmed flight routes. Humans only override the X-47B's programming if anomalies happen.
Source: http://www.fastcompany.com/3009724/inside-the-navys-historic-embrace-of-at-sea-combat-drones
Tuesday, May 14, 2013
Lithium-air battery four times as much energy per pound as today’s best lithium-ion batteries
Imaging reveals what happens during charging; could lead to improved batteries for electric cars.
One of the most promising new kinds of battery to power electric cars is called a lithium-air battery, which could store up to four times as much energy per pound as today’s best lithium-ion batteries.
Researchers at MIT and Sandia National Laboratories have used transmission electron microscope (TEM) imaging to observe, at a molecular level, what goes on during a reaction called oxygen evolution as lithium-air batteries charge; this reaction is thought to be a bottleneck limiting further improvements to these batteries. The TEM technique could help in finding ways to make such batteries practical in the near future.
The work is described in a Nano Letters paper by Robert Mitchell, who recently received a PhD in materials science and engineering from MIT; mechanical engineering PhD student Betar Gallant; Carl Thompson, the Stavros Salapatas Professor of Materials Science and Engineering; Yang Shao-Horn, the Gail E. Kendall Associate Professor of Mechanical Engineering and Materials Science and Engineering; and four other authors.
Faster charging
In fact, the rate of lithium peroxide oxidation in these experiments was approximately 100 times faster than the charging time for laboratory-scale lithium-air batteries, and approaches what is needed for applications. This demonstrates that if these batteries’ electron-transfer characteristics can be improved, it could allow for much faster charging while minimizing energy losses.
Source: http://web.mit.edu/newsoffice/2013/real-time-charging-of-lithium-air-battery-0513.html
One of the most promising new kinds of battery to power electric cars is called a lithium-air battery, which could store up to four times as much energy per pound as today’s best lithium-ion batteries.
Researchers at MIT and Sandia National Laboratories have used transmission electron microscope (TEM) imaging to observe, at a molecular level, what goes on during a reaction called oxygen evolution as lithium-air batteries charge; this reaction is thought to be a bottleneck limiting further improvements to these batteries. The TEM technique could help in finding ways to make such batteries practical in the near future.
The work is described in a Nano Letters paper by Robert Mitchell, who recently received a PhD in materials science and engineering from MIT; mechanical engineering PhD student Betar Gallant; Carl Thompson, the Stavros Salapatas Professor of Materials Science and Engineering; Yang Shao-Horn, the Gail E. Kendall Associate Professor of Mechanical Engineering and Materials Science and Engineering; and four other authors.
Faster charging
In fact, the rate of lithium peroxide oxidation in these experiments was approximately 100 times faster than the charging time for laboratory-scale lithium-air batteries, and approaches what is needed for applications. This demonstrates that if these batteries’ electron-transfer characteristics can be improved, it could allow for much faster charging while minimizing energy losses.
Source: http://web.mit.edu/newsoffice/2013/real-time-charging-of-lithium-air-battery-0513.html
Study IDs key protein for cell death
Findings may offer a new way to kill cancer cells by forcing them into an alternative programmed-death pathway.
When cells suffer too much DNA damage, they are usually forced to undergo programmed cell death, or apoptosis. However, cancer cells often ignore these signals, flourishing even after chemotherapy drugs have ravaged their DNA.
A new finding from MIT researchers may offer a way to overcome that resistance: The team has identified a key protein involved in an alternative death pathway known as programmed necrosis. Drugs that mimic the effects of this protein could push cancer cells that are resistant to apoptosis into necrosis instead.
“People really used to think of necrosis as cells just falling apart, that it wasn’t programmed and didn’t require gene products to make it happen,” says Leona Samson, a member of MIT’s Center for Environmental Health Sciences and Koch Institute for Integrative Cancer Research. “In the last few years it has become more clear that this is an active process that requires proteins to take place.”
In the May 10 online edition of the journal Genes and Development, Samson and colleagues report that a protein known as ALKBH7 plays a key role in controlling the programmed necrosis pathway. Dragony Fu, a former postdoc in Samson’s lab, is the paper’s lead author, and postdoc Jennifer Jordan is also an author.
In the new paper, Samson, a professor of biology and biological engineering, and her colleagues found that ALKBH7 has an unexpected effect. When the researchers lowered ALKBH7 levels in human cells grown in the lab, those cells were much more likely to survive DNA damage than cells with normal ALKBH7 levels. This suggests that ALKBH7 actually promotes cell death.
“That was a surprising finding, because previously all of these ALKBH proteins were shown to be helping the cell survive when exposed to damage,” says Fu, who is now a visiting research fellow at the University of Zurich.
Upon further investigation, the researchers found that when healthy cells suffer massive DNA damage from alkylating agents, they enter the programmed necrosis pathway. Necrosis, which can also be initiated by bacterial or viral infection, is believed to help the body’s immune system detect threats.
“When dying cells release their contents during necrosis, it serves as a warning signal for your body that there is a virus there and recruits macrophages and other immune cells to the area,” Fu says.
“The observations reported in this paper open up the possibility that novel treatments could be developed to treat tumors that are relatively resistant to killing via the apoptotic pathway,” says Ashok Bhagwat, a professor of chemistry at Wayne State University who was not part of the research team.
The research was funded by the National Institutes of Health and the American Cancer Society.
Source: http://web.mit.edu/newsoffice/2013/study-ids-key-protein-for-cell-death-0514.html
When cells suffer too much DNA damage, they are usually forced to undergo programmed cell death, or apoptosis. However, cancer cells often ignore these signals, flourishing even after chemotherapy drugs have ravaged their DNA.
A new finding from MIT researchers may offer a way to overcome that resistance: The team has identified a key protein involved in an alternative death pathway known as programmed necrosis. Drugs that mimic the effects of this protein could push cancer cells that are resistant to apoptosis into necrosis instead.
“People really used to think of necrosis as cells just falling apart, that it wasn’t programmed and didn’t require gene products to make it happen,” says Leona Samson, a member of MIT’s Center for Environmental Health Sciences and Koch Institute for Integrative Cancer Research. “In the last few years it has become more clear that this is an active process that requires proteins to take place.”
In the May 10 online edition of the journal Genes and Development, Samson and colleagues report that a protein known as ALKBH7 plays a key role in controlling the programmed necrosis pathway. Dragony Fu, a former postdoc in Samson’s lab, is the paper’s lead author, and postdoc Jennifer Jordan is also an author.
In the new paper, Samson, a professor of biology and biological engineering, and her colleagues found that ALKBH7 has an unexpected effect. When the researchers lowered ALKBH7 levels in human cells grown in the lab, those cells were much more likely to survive DNA damage than cells with normal ALKBH7 levels. This suggests that ALKBH7 actually promotes cell death.
“That was a surprising finding, because previously all of these ALKBH proteins were shown to be helping the cell survive when exposed to damage,” says Fu, who is now a visiting research fellow at the University of Zurich.
Upon further investigation, the researchers found that when healthy cells suffer massive DNA damage from alkylating agents, they enter the programmed necrosis pathway. Necrosis, which can also be initiated by bacterial or viral infection, is believed to help the body’s immune system detect threats.
“When dying cells release their contents during necrosis, it serves as a warning signal for your body that there is a virus there and recruits macrophages and other immune cells to the area,” Fu says.
“The observations reported in this paper open up the possibility that novel treatments could be developed to treat tumors that are relatively resistant to killing via the apoptotic pathway,” says Ashok Bhagwat, a professor of chemistry at Wayne State University who was not part of the research team.
The research was funded by the National Institutes of Health and the American Cancer Society.
Source: http://web.mit.edu/newsoffice/2013/study-ids-key-protein-for-cell-death-0514.html
Monday, May 06, 2013
Pilotless passenger planes prepare for take-off

Of course, the military already know this. Automatic landing systems have been used for years to help pilots drop F-18 aircraft on to the narrow landing strips on top of aircraft carriers. Then there is the rise of drone warfare. These planes are still flown remotely by pilots on the ground, but most have the capability to follow a predefined flight path and even land themselves if they get into serious trouble or the link between the ground is broken.
In some modern aircraft the pilot is only needed to taxi the aircraft to the runway. Everything else from take-off to landing can be automated. “The technology is here,” says Missy Cummings, an ex military pilot who is now associate professor at the Massachusetts Institute of Technology’s department of Aeronautics and Astronautics.
She points to the rise of so-called fly-by-wire technology, which has replaced the mechanical link between the pilot and the plane’s engines and control surfaces. “Any fly-by-wire plane can be an [Unmanned Aerial Vehicle],” she explains. “The controls are digital, not analogue, everything is done electronically so you don’t need a person in there to push a hydraulic actuator.”
To prove the point, technology company BAE Systems recently flew a converted Jetstream aircraft – known as “The Flying Test Bed” – with no pilot in UK air space.
A plane will need to be aware of its surroundings and be able to plot a new path that is not disruptive to other users of the skies - intelligence known as “sense and avoid”. Look at the rise of the autonomous car to see that computers are getting better and better at viewing an interpreting their surroundings.
Dr John Tracey, chief technology officer at Boeing, agrees. He sees no need for decisions to always be made on the ground by Air traffic Control. He believes the current system based on ground based radar, and a controller who uses voice commands to “say to the pilot ‘turn left, turn right, go up, go down,’” is very inefficient. “The new planes that we deliver already have the capabilities built into them to use GPS satellites, to allow them to fly on the most optimum flight path,” Dr Tracy says. The next step would be to allow aircraft to make more decisions for themselves and respond to other planes and weather patterns by themselves.
Professor Cummings says the data is increasingly in favour of unmanned systems. “About three years ago UAVs became safer than general aviation, meaning that more general aviation planes are crashing than UAVs, per 100,000 flight hours,” she says. “So UAVs are actually safer than a weekend pilot, flying a small plane.”
Update from article newscientist:
Jim Scanlan, one of the designers of the world's first 3D-printed unmanned aerial vehicle is impressed. "I think it's great. It's good to see such progress in the UK – especially with the US hoping to open up its airspace to UAVs in 2015."
The main thing ASTRAEA needs to get right is that sensing and avoiding capability, says Scanlan. "That's the showstopper at the moment. Without a pilot they need a sensing system to replace the Mark 1 eyeball – one that can tell a hot-air balloon from a cloud."
Source:
http://www.bbc.com/future/story/20130502-pilotless-planes-plan-to-take-off/1
http://www.newscientist.com/article/dn23521-passenger-jet-flies-800-kilometres-without-a-pilot.html
Wednesday, May 01, 2013
Unleashing oxygen
‘Superlattice’ structure could give a huge boost to oxygen reaction in fuel cells, increasing their power potential.
New research at MIT could dramatically improve the efficiency of fuel cells, which are considered a promising alternative to batteries for powering everything from electronic devices to cars and homes.
Now that the MIT team has analysed LSC113/214, it may be possible to discover even better materials by conducting systematic searches, Yildiz says; the team is now working on that. “If we can crack this problem, then we can make great strides in improving the performance,” adds Tuller, a professor of ceramics and electronic materials in MIT’s Department of Materials Science and Engineering.
Source: http://web.mit.edu/newsoffice/2013/superlattice-could-boost-fuel-cell-performance-0430.html#.UYEEy6aZqe4.blogger
New research at MIT could dramatically improve the efficiency of fuel cells, which are considered a promising alternative to batteries for powering everything from electronic devices to cars and homes.
Now that the MIT team has analysed LSC113/214, it may be possible to discover even better materials by conducting systematic searches, Yildiz says; the team is now working on that. “If we can crack this problem, then we can make great strides in improving the performance,” adds Tuller, a professor of ceramics and electronic materials in MIT’s Department of Materials Science and Engineering.
Tuesday, April 23, 2013
A different view of cancer cells
New study measures physical changes in tumor cells as they become metastatic.
Most cancer deaths are caused by metastatic tumors, which break free from the original cancer site and spread throughout the body. For that to happen, cancer cells must undergo many genetic and physical changes. Now, MIT researchers have developed a way to study three key physical properties of cancer cells — their mass, stiffness and friction — on a large scale.
Using this system, the researchers have analyzed how changes in those traits may allow cancer cells to migrate to new sites: Scientists have previously observed that cell lines with higher metastatic potential are generally more deformable, but the MIT team found that decreased friction also appears to help cancer cells traverse narrow channels, suggesting that friction may play a role in the ability of cancer cells to travel in blood vessels and reach new tumor sites.
“Our measurements provide an additional perspective on cell properties that may complement genomic and proteomic approaches,” says Sangwon Byun, an MIT postdoc and lead author of a paper describing the findings in the Proceedings of the National Academy of Sciences the week of April 22.
The system that Byun and colleagues used to study the cancer cells is based on a device previously developed by Scott Manalis, a member of MIT's Koch Institute for Integrative Cancer Research and an MIT professor of biological engineering. Manalis, the senior author of the PNAS paper, has previously demonstrated that this system, known as a suspended microchannel resonator (SMR), can very accurately measure the mass and density of individual cells.
The new MIT system is “probably the world’s most sensitive instrument for measuring a number of different biophysical properties of individual cells,” says Mehmet Toner, a professor of biomedical engineering at Massachusetts General Hospital and Harvard Medical School who was not part of the research team. “It’s very important to know whether metastatic cells have biophysical properties different than normal or nonmetastatic cancer cells, allowing them to go through narrow spaces.”
“When you use a specific marker to look for these cells, you find the cells that you’re looking for, but you may be missing a whole population of cells,” says Josephine Shaw, an MIT graduate student and a co-author of the paper. “It’s possible that by using a more holistic and physical approach, we may be able to find certain cells that we wouldn’t be able to find molecularly, because we wouldn’t be able to guess ahead of time what these cells would be expressing.”
Other authors of the paper are MIT postdoc Sungmin Son; Stanford University postdoc Dario Amodei; MIT grad students Nathan Cermak, Joon Ho Kang and Vivian Hecht; former MIT postdoc Monte Winslow; Tyler Jacks, the David H. Koch Professor of Biology at MIT and director of the Koch Institute; and Parag Mallick, an assistant professor of radiology at Stanford.
The research was funded by the National Cancer Institute, through MIT’s Physical Sciences Oncology Center and Stanford’s Center for Cancer Nanotechnology Excellence and Translation, and Stand Up to Cancer.
Friday, April 19, 2013
Major boost in solar-cell efficiency
Throughout decades of research on solar cells, one formula has been considered an absolute limit to the efficiency of such devices in converting sunlight into electricity: Called the Shockley-Queisser efficiency limit, it posits that the ultimate conversion efficiency can never exceed 34 percent for a single optimized semiconductor junction.
Now, researchers at MIT have shown that there is a way to blow past that limit as easily as today’s jet fighters zoom through the sound barrier — which was also once seen as an ultimate limit.
Their work appears this week in a report in the journal Science, co-authored by graduate students including Daniel Congreve, Nicholas Thompson, Eric Hontz and Shane Yost, alumna Jiye Lee ’12, and professors Marc Baldo and Troy Van Voorhis.
Since this was just a first proof of principle, the team has not yet optimized the energy-conversion efficiency of the system, which remains less than 2 percent. But ratcheting up that efficiency through further optimization should be a straightforward process, the researchers say. “There appears to be no fundamental barrier,” Thompson says.
While today’s commercial solar panels typically have an efficiency of at most 25 percent, a silicon solar cell harnessing singlet fission should make it feasible to achieve efficiency of more than 30 percent, Baldo says — a huge leap in a field typically marked by slow, incremental progress. In solar cell research, he notes, people are striving “for an increase of a tenth of a percent.”
Solar panel efficiencies can also be improved by stacking different solar cells together, but combining solar cells is expensive with conventional solar-cell materials. The new technology instead promises to work as an inexpensive coating on solar cells.
Friday, April 12, 2013
Robot truck platoons roll forward
Will this be the first step toward autonomous cars?
Convoys of wireless-linked semi-autonomous vehicles could soon be hitting our roads, giving drivers a chance to put their feet up on the morning commute.
In February this year, a similar line-up of four large trucks circled an oval test track in Tsukuba City, Japan to help get so-called “truck platooning” technology ready for real-world use. This technology aims to create semi-autonomous road trains, where convoys of vehicles enter a snaking train of vehicles under the command of the lead vehicle.
“We think that this new technology can also lead to a reduction in the amount of road space used by vehicles, which would help to reduce traffic congestion,” says Nobuo Iwai, senior researcher on the project. In fact, some estimates suggest it could double the capacity of existing highways.
Platoon prototype
The Japanese demonstration was the latest of a couple of projects set up to trial and develop the technology. A couple of years ago a project at RWTH Aachen University in Germany operated a platoon of four trucks spaced at 10m (33ft) intervals. In the US, research at the University of California, Berkeley put three-truck caravans on the road with spacing from 3 to 6m. And last year, the Scania Transport Laboratory in Swedentested aspects of truck platooning on a 520km (325 miles) shipping route between the cities of Sodertalje and Helsingborg.
In addition, a recently completed European project led by Volvo calledSafe Road Trains for the Environment (Sartre) has explored using cars and lorries simultaneously. Its platoons cruised at 85 km/h (50mph) with a gap between each vehicle of 6m. The study vehicles put in some 10,000 km (6,200 miles) of road, and – like the Japanese study – indicated that platooning could offer substantial benefits.
Engineers and planners working on the technology that road trains could be cruising highways sometime in the next decade. Perhaps in the not-too-distant future, you yourself will commute to work on a robotic conga line, along with a line up of other drivers not paying attention to driving.
Source: http://www.bbc.com/future/story/20130409-robot-truck-platoons-roll-forward/2
Convoys of wireless-linked semi-autonomous vehicles could soon be hitting our roads, giving drivers a chance to put their feet up on the morning commute.
In February this year, a similar line-up of four large trucks circled an oval test track in Tsukuba City, Japan to help get so-called “truck platooning” technology ready for real-world use. This technology aims to create semi-autonomous road trains, where convoys of vehicles enter a snaking train of vehicles under the command of the lead vehicle.
“We think that this new technology can also lead to a reduction in the amount of road space used by vehicles, which would help to reduce traffic congestion,” says Nobuo Iwai, senior researcher on the project. In fact, some estimates suggest it could double the capacity of existing highways.
Platoon prototype
The Japanese demonstration was the latest of a couple of projects set up to trial and develop the technology. A couple of years ago a project at RWTH Aachen University in Germany operated a platoon of four trucks spaced at 10m (33ft) intervals. In the US, research at the University of California, Berkeley put three-truck caravans on the road with spacing from 3 to 6m. And last year, the Scania Transport Laboratory in Swedentested aspects of truck platooning on a 520km (325 miles) shipping route between the cities of Sodertalje and Helsingborg.
In addition, a recently completed European project led by Volvo calledSafe Road Trains for the Environment (Sartre) has explored using cars and lorries simultaneously. Its platoons cruised at 85 km/h (50mph) with a gap between each vehicle of 6m. The study vehicles put in some 10,000 km (6,200 miles) of road, and – like the Japanese study – indicated that platooning could offer substantial benefits.
Engineers and planners working on the technology that road trains could be cruising highways sometime in the next decade. Perhaps in the not-too-distant future, you yourself will commute to work on a robotic conga line, along with a line up of other drivers not paying attention to driving.
Source: http://www.bbc.com/future/story/20130409-robot-truck-platoons-roll-forward/2
Wednesday, April 10, 2013
'Aggressive' prostate cancer gene find
The BRCA2 gene is linked to hereditary breast cancer, as well as prostate and ovarian cancer.
Now scientists say that as well as being more likely to get prostate cancer, men with BRCA2 are also more likely to develop aggressive tumours and have the poorest survival rates.
They say these men should be treated quickly to save lives.
Prof Ros Eeles and colleagues at The Institute of Cancer Research in London and The Royal Marsden NHS Foundation Trust found prostate cancers spread more quickly and were more often fatal in men who had inherited a faulty BRCA2 gene than in men without the faulty gene.
Prof Eeles said: "It is clear from our study that prostate cancers linked to inheritance of the BRCA2 cancer gene are more deadly than other types.
"It must make sense to start offering affected men immediate surgery or radiotherapy, even for early-stage cases that would otherwise be classified as low-risk.
Men with a significant family history of breast and/or ovarian cancer in addition to prostate cancer can be offered BRCA1/2 testing at diagnosis, but it is not routinely offered to all patients diagnosed with prostate cancer in the UK.
Dr Julie Sharp of Cancer Research UK, said: "This study shows that doctors need to consider treating men with prostate cancer and a faulty BRCA2 gene much sooner than they currently do, rather than waiting to see how the disease develops.
Source: http://www.bbc.co.uk/news/health-22065289
Now scientists say that as well as being more likely to get prostate cancer, men with BRCA2 are also more likely to develop aggressive tumours and have the poorest survival rates.
They say these men should be treated quickly to save lives.
Prof Ros Eeles and colleagues at The Institute of Cancer Research in London and The Royal Marsden NHS Foundation Trust found prostate cancers spread more quickly and were more often fatal in men who had inherited a faulty BRCA2 gene than in men without the faulty gene.
Prof Eeles said: "It is clear from our study that prostate cancers linked to inheritance of the BRCA2 cancer gene are more deadly than other types.
"It must make sense to start offering affected men immediate surgery or radiotherapy, even for early-stage cases that would otherwise be classified as low-risk.
Men with a significant family history of breast and/or ovarian cancer in addition to prostate cancer can be offered BRCA1/2 testing at diagnosis, but it is not routinely offered to all patients diagnosed with prostate cancer in the UK.
Dr Julie Sharp of Cancer Research UK, said: "This study shows that doctors need to consider treating men with prostate cancer and a faulty BRCA2 gene much sooner than they currently do, rather than waiting to see how the disease develops.
Source: http://www.bbc.co.uk/news/health-22065289
Subscribe to:
Posts (Atom)