Filipino Physicists Awarded a US Patent for a New Semiconductor Circuit Imaging Technique
A microscope imaging technique for visualizing and analyzing semiconductor integrated circuits developed by a team of scientists from the University of the Philippines’ National Institute of Physics was awarded a patent by the United States Patent and Trademark Office.
Imagine if our computers, cellular phones and other electronic gadgets cease to work due to failures in the circuits that run them. These failures in the minuscule wires that make up the semiconductor integrated circuits embedded in our electronic products must be detected in order to make sure that our prized gadgets function. To detect such failures, an effective technique for visualizing and analyzing circuits has been developed by a team of scientists from the University of the Philippines’ National Institute of Physics (UP NIP), namely: Dr. Ceasar Saloma, Dr. Vincent Ricardo M. Daria and Ms. Jelda Jane C. Miranda. This microscope imaging technique entitled “Method for Generating High Contrast Images of Semiconductor Sites via One-Photon Optical Beam-induced Current (IP OBIC) Imaging and Confocal Reflectance Microscopy” was awarded a patent by the United States Patent and Trademark Office last June 26, 2007.
Saloma, currently Dean of the College of Science of the University of the Philippines, is recipient of prestigious international awards for outstanding scientific work, among them the Galileo Galilei Award from the International Commission on Optics. Daria, Associate Professor at the UP-NIP is one of its most active researchers, and Miranda, who was part of its Experimental Optics Group now works for Intel Corporation. The US patent gives Saloma and his team an exclusive right to commercialize their invention in the United States without fear of infringement. The patent is effective for 20 years after the filing of application in December 09, 2006. For more details on the invention, you may check out the United States Patents and Trademarks Office website at http://patft.uspto.gov/.
The invention combines two existing imaging techniques called confocal reflectance microscopy and 1P-OBIC. It uses computer software to produce a high-contrast image mapping of the semiconductor and metal sites in an integrated circuit. The technique is a major breakthrough in the semiconductor industry. It is particularly useful in the manufacturing of microprocessors, integrated circuits and memories for computers, cellular phones and other electronic devices. Creating sharp visual images of semiconductor integrated circuits is important for failure analysis since one can track which part of the device would produce electrical current when hit by laser beam. The method facilitates accurate identification of semiconductor and metal sites in an integrated circuit. With this technique, defects in the circuit can be detected, thus ensuring quality control of such devices.
The main claims of the patent include a description of a technique that facilitates discrimination of these two types of materials in an integrated circuit. The claims also include a description of the optical layout for a generic confocal microscope that allows for simultaneous acquisition of reflectance confocal image and single-photon optical beam induced current (OBIC) image. Moreover, the patent includes an algorithm and software control for microscopic image acquisition for both confocal and OBIC image.
Applications of the patent extend to a fully integrated microscope system for failure analysis of integrated circuits by improved visualization and mapping of materials in a semiconductor device. The microscope extends to a system for measuring optical beam induced current of semiconductor materials. Further applications of the patent may include the construction of a general purpose Confocal Reflectance microscope system for viewing microscopic objects.
Just last March 16, 2007, another scientist from the National Institute of Physics in the University of the Philippines, Dr. Henry J. Ramos, was awarded a Taiwan patent for his invention entitled “Titanium Nitride Thin Formation on Metal Substrate by Chemical Vapor Deposition in a Magnetized Sheet Plasma Source.” The invention has a wide range of applications: cutting tools manufacturing, and the production of aerospace components, marine hardware, medical devices, and pharmaceutical equipment among others.
-By Jennalyn S. Baraquio and Agnes A. Paculdar
Saturday, July 28, 2007
Breaking the frustration
The crystal structure of an oxide material is directly coupled to its ‘frustrated’ magnetic structure
Researchers from the RIKEN SPring-8 Center in Harima, the Japan Atomic Energy Agency and the universities of Tokyo and Virginia have discovered how changes to the crystal structure of the oxide material HgCr2O4 correlate to its magnetic state.
HgCr2O4 has an intriguing crystal structure where all relevant atoms are arranged in tetrahedra (Fig. 1 - Click on link below). When the interaction between the magnetic atoms at the corners of these tetrahedra is antiferromagnetic, a magnetic state with a zero net ‘moment’ is expected to occur—that is, there should be as many magnetic arrows pointing upwards as downwards. However, the geometry of the tetrahedra means that no perfectly homogeneous distribution of the moments is possible. This is known as ‘geometrically frustrated magnetism’.
To break the frustration, the system compensates for the uneven distribution of magnetic moments by distorting the crystal lattice (Fig. 1a). However, in response to an increasing external magnetic field, the magnetic moments realign and there is a stepwise reduction in crystal distortion (Fig. 1b). Once all magnetic moments are forced to point in the same direction, a perfectly symmetric crystal structure is assumed (Fig. 1c).
As reported in the journal Nature Physics (1), the research team studied the behavior of this material as they applied a slowly increasing magnetic field. They confirmed that the external magnetic field eventually breaks the zero magnetization of the sample and causes the magnetic spins to align along the external field—evidenced by sudden jumps in the sample magnetization followed by plateaus with constant magnetization.
Unlike other materials, HgCr2O4 is uniquely suited for this type of study, as these changes occur in magnetic fields small enough to be generated in experiments. Therefore, “the observation of magnetization plateaus in this compound over a wide range of magnetic fields is novel and a manifestation of the geometrical frustration,” explains Koichi Katsumata from the RIKEN team.
Importantly, the researchers studied for the first time the simultaneous evolution of the material’s crystal structure and found that as the magnetization jumps between the different plateaus, the crystal structure becomes less distorted (Fig. 1). Katsumata is therefore confident that this study “has unveiled the origin of some of the intriguing properties of geometrically frustrated magnets.” In particular, the results allow the validation and refinement of theoretical models describing the interaction between magnetism and crystal structure not only in this compound, but also in related systems.
Reference
1. Matsuda, M., Ueda, H., Kikkawa, A., Tanaka, Y., Katsumata, K., Narumi, Y., Inami, T., Ueda, Y. & Lee, S.-H. Spin-lattice instability to a fractional magnetization state in the spinel HgCr2O4. Nature Physics 3, 397–400 (2007).
The crystal structure of an oxide material is directly coupled to its ‘frustrated’ magnetic structure
Researchers from the RIKEN SPring-8 Center in Harima, the Japan Atomic Energy Agency and the universities of Tokyo and Virginia have discovered how changes to the crystal structure of the oxide material HgCr2O4 correlate to its magnetic state.
HgCr2O4 has an intriguing crystal structure where all relevant atoms are arranged in tetrahedra (Fig. 1 - Click on link below). When the interaction between the magnetic atoms at the corners of these tetrahedra is antiferromagnetic, a magnetic state with a zero net ‘moment’ is expected to occur—that is, there should be as many magnetic arrows pointing upwards as downwards. However, the geometry of the tetrahedra means that no perfectly homogeneous distribution of the moments is possible. This is known as ‘geometrically frustrated magnetism’.
To break the frustration, the system compensates for the uneven distribution of magnetic moments by distorting the crystal lattice (Fig. 1a). However, in response to an increasing external magnetic field, the magnetic moments realign and there is a stepwise reduction in crystal distortion (Fig. 1b). Once all magnetic moments are forced to point in the same direction, a perfectly symmetric crystal structure is assumed (Fig. 1c).
As reported in the journal Nature Physics (1), the research team studied the behavior of this material as they applied a slowly increasing magnetic field. They confirmed that the external magnetic field eventually breaks the zero magnetization of the sample and causes the magnetic spins to align along the external field—evidenced by sudden jumps in the sample magnetization followed by plateaus with constant magnetization.
Unlike other materials, HgCr2O4 is uniquely suited for this type of study, as these changes occur in magnetic fields small enough to be generated in experiments. Therefore, “the observation of magnetization plateaus in this compound over a wide range of magnetic fields is novel and a manifestation of the geometrical frustration,” explains Koichi Katsumata from the RIKEN team.
Importantly, the researchers studied for the first time the simultaneous evolution of the material’s crystal structure and found that as the magnetization jumps between the different plateaus, the crystal structure becomes less distorted (Fig. 1). Katsumata is therefore confident that this study “has unveiled the origin of some of the intriguing properties of geometrically frustrated magnets.” In particular, the results allow the validation and refinement of theoretical models describing the interaction between magnetism and crystal structure not only in this compound, but also in related systems.
Reference
1. Matsuda, M., Ueda, H., Kikkawa, A., Tanaka, Y., Katsumata, K., Narumi, Y., Inami, T., Ueda, Y. & Lee, S.-H. Spin-lattice instability to a fractional magnetization state in the spinel HgCr2O4. Nature Physics 3, 397–400 (2007).
Take your computer for a spin
RIKEN Large spin Hall effect measured at room temperature
RIKEN scientists have accurately measured a tiny voltage produced by segregating electrons according to their spin (1), a result which could help to usher in a new era of spin-based computing.
Conventional computers process and communicate information by shunting electrons around, but store data in the magnetic properties of tiny segments of a spinning disk drive. Yet that magnetism is also due to electrons—as each charged particle spins, it creates a magnetic moment. Electrons can spin ‘up’ or ‘down’, creating opposing poles like a bar magnet, and the burgeoning technology of spintronics uses these two states to represent bits of binary data. As well as storing information, these states can potentially be used to perform calculations.
The spin Hall effect (SHE) provides an important way to control these spinning electrons. The Hall effect itself (identified in 1879 by Edwin Hall) occurs when a magnetic field forces a current of electrons flowing through a flat plate to veer to one side. This causes charge to accumulate on that side of the plate, setting up a voltage across it. In a similar way, the SHE sends spin-up electrons to one side of the plate and spin-down to the other, setting up a ‘spin current’ (Fig. 1 - Click on link below).
Spin current is an important factor in operating future spintronic devices. Ferromagnets are normally used to differentiate spins, but interference between neighboring magnets makes it tricky to build working spintronic devices that way.
“However, if we use SHE, we can generate the spin current without using a ferromagnet,” says Takashi Kimura of RIKEN’s Frontier Research System, Wako. This could allow much easier integration of semiconductor and spintronic devices in the future.
Kimura and the team leader YoshiChika Otani have now found that the spin Hall conductivity—the potential for electrons to migrate due to the SHE—in a platinum wire is a thousand times greater than in previous experiments with semiconductor materials, making it easier to study and exploit the effect. Their electrical measurement technique is also more precise than the optical detection method usually employed.
It’s significant that the team has detected this effect at room temperature. It means that SHE is not only a physically interesting phenomenon, but also a useful way of manipulating spins in future spintronic devices, says Kimura.
The team is now trying to identify materials that produce even greater SHE conductivities. “We hope that new devices using SHE are proposed in near future,” says Kimura.
Reference
1. Kimura, T., Otani, Y., Sato, T., Takahashi, S. & Maekawa, S. Room-temperature reversible spin Hall effect. Physical Review Letters 98, 156601 (2007).
RIKEN Large spin Hall effect measured at room temperature
RIKEN scientists have accurately measured a tiny voltage produced by segregating electrons according to their spin (1), a result which could help to usher in a new era of spin-based computing.
Conventional computers process and communicate information by shunting electrons around, but store data in the magnetic properties of tiny segments of a spinning disk drive. Yet that magnetism is also due to electrons—as each charged particle spins, it creates a magnetic moment. Electrons can spin ‘up’ or ‘down’, creating opposing poles like a bar magnet, and the burgeoning technology of spintronics uses these two states to represent bits of binary data. As well as storing information, these states can potentially be used to perform calculations.
The spin Hall effect (SHE) provides an important way to control these spinning electrons. The Hall effect itself (identified in 1879 by Edwin Hall) occurs when a magnetic field forces a current of electrons flowing through a flat plate to veer to one side. This causes charge to accumulate on that side of the plate, setting up a voltage across it. In a similar way, the SHE sends spin-up electrons to one side of the plate and spin-down to the other, setting up a ‘spin current’ (Fig. 1 - Click on link below).
Spin current is an important factor in operating future spintronic devices. Ferromagnets are normally used to differentiate spins, but interference between neighboring magnets makes it tricky to build working spintronic devices that way.
“However, if we use SHE, we can generate the spin current without using a ferromagnet,” says Takashi Kimura of RIKEN’s Frontier Research System, Wako. This could allow much easier integration of semiconductor and spintronic devices in the future.
Kimura and the team leader YoshiChika Otani have now found that the spin Hall conductivity—the potential for electrons to migrate due to the SHE—in a platinum wire is a thousand times greater than in previous experiments with semiconductor materials, making it easier to study and exploit the effect. Their electrical measurement technique is also more precise than the optical detection method usually employed.
It’s significant that the team has detected this effect at room temperature. It means that SHE is not only a physically interesting phenomenon, but also a useful way of manipulating spins in future spintronic devices, says Kimura.
The team is now trying to identify materials that produce even greater SHE conductivities. “We hope that new devices using SHE are proposed in near future,” says Kimura.
Reference
1. Kimura, T., Otani, Y., Sato, T., Takahashi, S. & Maekawa, S. Room-temperature reversible spin Hall effect. Physical Review Letters 98, 156601 (2007).
Saturday, July 14, 2007
A concerted effort : proton transfer in a chemical reaction
Chemical reactions are processes in which one substance is transformed into another and involve the motion of atoms and electrons. Because these processes occur on short time-scales that are measured in femtoseconds (millionths of a billionth of a second), it is difficult to study what actually happens during a chemical reaction.
Of particular interest are reactions that involve the transfer of a hydrogen nucleus (a proton) between two molecules—an important process in biological systems. Tahei Tahara from RIKEN’s Discovery Research Institute in Wako has been studying proton transfer reactions for many years and views them as a challenge at the limits of science. “Because hydrogen is the lightest atomic species, it usually moves very quickly and is difficult to catch,” comments Tahara.
A model system in which proton transfer has been extensively studied is 7-azaindole. In solution, this compound exists in two different forms; discrete individual molecules (monomers), and pairs known as dimers. The dimers can be pushed into a higher energy ‘excited’ state by shining ultraviolet light on them, and subsequently undergo a double proton transfer reaction to form a structure known as a tautomer.
When Tahara published his first results on this system ten years ago, he says that, “the work triggered very intense world-wide debate.” The controversy stemmed from whether the two proton-transfer steps occurred sequentially in a step-wise reaction, or simultaneously in a ‘concerted’ process. Tahara has always argued that the concerted process is the correct one, a hypothesis that is further supported by his recent findings published in the Proceedings of the National Academy of Sciences of the USA (1).
By exciting the 7-azaindole dimer with different wavelengths of ultraviolet light and monitoring the fluorescence, Tahara and colleague, Satoshi Takeuchi, show conclusively that no intermediate structure is formed, thereby ruling out the possibility of a step-wise process. Significantly, their experiments demonstrate that a feature of the fluorescence decay that was attributed to a separate proton transfer actually corresponds to the conversion of the dimer from one excited state to another.
Because the 7-azaindole dimer is very similar in structure to the base pairs found in DNA, Tahara expects that this work may help to understand the chemical mechanism of how ultraviolet light affects DNA. In addition, Tahara and co-workers are now intending to observe nuclear motion in real-time using sub-10-femtosecond pulses of light, which he suggests, “may offer new opportunities for using light to control chemical reactions.”
Chemical reactions are processes in which one substance is transformed into another and involve the motion of atoms and electrons. Because these processes occur on short time-scales that are measured in femtoseconds (millionths of a billionth of a second), it is difficult to study what actually happens during a chemical reaction.
Of particular interest are reactions that involve the transfer of a hydrogen nucleus (a proton) between two molecules—an important process in biological systems. Tahei Tahara from RIKEN’s Discovery Research Institute in Wako has been studying proton transfer reactions for many years and views them as a challenge at the limits of science. “Because hydrogen is the lightest atomic species, it usually moves very quickly and is difficult to catch,” comments Tahara.
A model system in which proton transfer has been extensively studied is 7-azaindole. In solution, this compound exists in two different forms; discrete individual molecules (monomers), and pairs known as dimers. The dimers can be pushed into a higher energy ‘excited’ state by shining ultraviolet light on them, and subsequently undergo a double proton transfer reaction to form a structure known as a tautomer.
When Tahara published his first results on this system ten years ago, he says that, “the work triggered very intense world-wide debate.” The controversy stemmed from whether the two proton-transfer steps occurred sequentially in a step-wise reaction, or simultaneously in a ‘concerted’ process. Tahara has always argued that the concerted process is the correct one, a hypothesis that is further supported by his recent findings published in the Proceedings of the National Academy of Sciences of the USA (1).
By exciting the 7-azaindole dimer with different wavelengths of ultraviolet light and monitoring the fluorescence, Tahara and colleague, Satoshi Takeuchi, show conclusively that no intermediate structure is formed, thereby ruling out the possibility of a step-wise process. Significantly, their experiments demonstrate that a feature of the fluorescence decay that was attributed to a separate proton transfer actually corresponds to the conversion of the dimer from one excited state to another.
Because the 7-azaindole dimer is very similar in structure to the base pairs found in DNA, Tahara expects that this work may help to understand the chemical mechanism of how ultraviolet light affects DNA. In addition, Tahara and co-workers are now intending to observe nuclear motion in real-time using sub-10-femtosecond pulses of light, which he suggests, “may offer new opportunities for using light to control chemical reactions.”
Researchers find a gene controlling embryo orientation
Developmental biologists from RIKEN working with Japanese and Canadian colleagues have located an important gene that regulates the establishment of the head-to-tail or anterior-to-posterior (A–P) axis in mice. The future development of the whole embryo is orientated to this point of reference.
The A–P axis appears before the emergence of the three primary germ layers of body tissue during the process known as gastrulation, when the primitive ball of cells called the blastula folds in on itself to form the more complex, layered structure of the gastrula. Before gastrulation, there are only two types of tissue—epiblast from which the animal proper develops and visceral endoderm (VE) that forms all of the support structures such as blood vessels and nutrient cells.
The establishment of the A–P axis involves interplay between the VE cells and the underlying epiblast. In particular, a group of VE cells furthest from where embryonic structure attaches to the uterus migrates to close to where the head will develop in the epiblast. At the same time VE cells near the posterior end of the axis switch on a gene, Wnt, that produces a compound necessary to initiate gastrulation. In contrast, the VE cells at the head end or anterior visceral endoderm (AVE) produce compounds which block Wnt.
Earlier work has shown that the developmental gene known as Otx2 is critical in the generation and function of the AVE. In mutants lacking Otx2 there is no migration of VE cells to form the AVE and a key antagonist to Wnt is not produced. But the factors that regulated Otx2 were unknown.
In a recent paper in the Proceedings of the National Academy of Sciences (1), the researchers from RIKEN’s Center for Developmental Biology in Kobe and their colleagues describe how they used carefully engineered transgenic mice to demonstrate the critical role of the transcription factor Foxa2 in regulating Otx2. In laboratory studies, they also showed that the Foxa2 protein is needed for the production of at least two Wnt antagonists. Through these actions Foxa2 controls the establishment of the A–P axis.
Similar genes and compounds also exist in the pufferfish, fugu (Fig. 1 - Click on link). In fact, the group found, the fugu equivalent of Foxa2 can actually work in mice. According to the researchers, this shows how tightly the whole regulatory system has been conserved in the evolution of higher vertebrates from the bony fishes.
Reference
Developmental biologists from RIKEN working with Japanese and Canadian colleagues have located an important gene that regulates the establishment of the head-to-tail or anterior-to-posterior (A–P) axis in mice. The future development of the whole embryo is orientated to this point of reference.
The A–P axis appears before the emergence of the three primary germ layers of body tissue during the process known as gastrulation, when the primitive ball of cells called the blastula folds in on itself to form the more complex, layered structure of the gastrula. Before gastrulation, there are only two types of tissue—epiblast from which the animal proper develops and visceral endoderm (VE) that forms all of the support structures such as blood vessels and nutrient cells.
The establishment of the A–P axis involves interplay between the VE cells and the underlying epiblast. In particular, a group of VE cells furthest from where embryonic structure attaches to the uterus migrates to close to where the head will develop in the epiblast. At the same time VE cells near the posterior end of the axis switch on a gene, Wnt, that produces a compound necessary to initiate gastrulation. In contrast, the VE cells at the head end or anterior visceral endoderm (AVE) produce compounds which block Wnt.
Earlier work has shown that the developmental gene known as Otx2 is critical in the generation and function of the AVE. In mutants lacking Otx2 there is no migration of VE cells to form the AVE and a key antagonist to Wnt is not produced. But the factors that regulated Otx2 were unknown.
In a recent paper in the Proceedings of the National Academy of Sciences (1), the researchers from RIKEN’s Center for Developmental Biology in Kobe and their colleagues describe how they used carefully engineered transgenic mice to demonstrate the critical role of the transcription factor Foxa2 in regulating Otx2. In laboratory studies, they also showed that the Foxa2 protein is needed for the production of at least two Wnt antagonists. Through these actions Foxa2 controls the establishment of the A–P axis.
Similar genes and compounds also exist in the pufferfish, fugu (Fig. 1 - Click on link). In fact, the group found, the fugu equivalent of Foxa2 can actually work in mice. According to the researchers, this shows how tightly the whole regulatory system has been conserved in the evolution of higher vertebrates from the bony fishes.
Reference
Playing tag highlights genetic disorder
A team of Japanese scientists led by Akimitsu Okamoto from the RIKEN Frontier Research System, Wako, has developed a new method for tagging a particular DNA base responsible for causing cancer.
Cytosine, a common DNA base, is reacted to add a methyl group to form methylcytosine during many biological processes. This process, known as methylation, is important for gene regulation, and DNA and protein stability. Further, excessive methylation of cytosine has been shown to result in cancer. The development of simple techniques to detect methylcytosine is therefore of great interest to scientists.
Although conventional methods have many advantages, they also have problems. Current methods cannot differentiate between cytosine and methylcytosine; they also destroy the DNA sample and are time-consuming. The latest technique by Okamoto and co-workers is selective for methylcytosine, fast and allows easy detection1.
The technique takes advantage of the easy oxidation of methylcytosine and uses three, specially designed, components to enable detection. When the reaction takes place, the methylcytosine forms a stable complex with an oxidant, potassium osmate, and a rate-enhancing ligand. The ligand, a bipyridine derivative, can then react further to bond with a variety of fluorescent or electrochemical tags allowing routine detection of the complex (Fig. 1 - Click on link below).
This conceptually new approach to methylcytosine detection takes just six hours to complete. Importantly, the key complex only forms between the methylcytosine and the ligand. This leaves the cytosine in the sample untouched and allows a clear distinction to be made. In addition, methylcytosines in single-stranded DNA efficiently formed the complex, whereas complexation of methylcytosines in a DNA duplex was suppressed. This result implies that the technique could also provide sequence-specific results giving detailed and accurate information of the methylated sites.
Okamoto explains that there is still more work to be done. Unfortunately, the information gained from the sequence-specific studies is limited as a consequence of the competing reaction with thymine, another DNA base. Also, the signal intensities and sensitivities are a little too weak to be useful on small sample sizes at this time.
Okamoto and his team are now striving to improve their technique so it can be used routinely in clinics with standard fluorescence or electronic signal analyzers. This technique is based on easy-to-use chemistry and Okamoto says, “Because the total process finishes in a few hours, this technique may make it possible to design machines that automate a series of processes from purification of samples to analysis.”
Reference
A team of Japanese scientists led by Akimitsu Okamoto from the RIKEN Frontier Research System, Wako, has developed a new method for tagging a particular DNA base responsible for causing cancer.
Cytosine, a common DNA base, is reacted to add a methyl group to form methylcytosine during many biological processes. This process, known as methylation, is important for gene regulation, and DNA and protein stability. Further, excessive methylation of cytosine has been shown to result in cancer. The development of simple techniques to detect methylcytosine is therefore of great interest to scientists.
Although conventional methods have many advantages, they also have problems. Current methods cannot differentiate between cytosine and methylcytosine; they also destroy the DNA sample and are time-consuming. The latest technique by Okamoto and co-workers is selective for methylcytosine, fast and allows easy detection1.
The technique takes advantage of the easy oxidation of methylcytosine and uses three, specially designed, components to enable detection. When the reaction takes place, the methylcytosine forms a stable complex with an oxidant, potassium osmate, and a rate-enhancing ligand. The ligand, a bipyridine derivative, can then react further to bond with a variety of fluorescent or electrochemical tags allowing routine detection of the complex (Fig. 1 - Click on link below).
This conceptually new approach to methylcytosine detection takes just six hours to complete. Importantly, the key complex only forms between the methylcytosine and the ligand. This leaves the cytosine in the sample untouched and allows a clear distinction to be made. In addition, methylcytosines in single-stranded DNA efficiently formed the complex, whereas complexation of methylcytosines in a DNA duplex was suppressed. This result implies that the technique could also provide sequence-specific results giving detailed and accurate information of the methylated sites.
Okamoto explains that there is still more work to be done. Unfortunately, the information gained from the sequence-specific studies is limited as a consequence of the competing reaction with thymine, another DNA base. Also, the signal intensities and sensitivities are a little too weak to be useful on small sample sizes at this time.
Okamoto and his team are now striving to improve their technique so it can be used routinely in clinics with standard fluorescence or electronic signal analyzers. This technique is based on easy-to-use chemistry and Okamoto says, “Because the total process finishes in a few hours, this technique may make it possible to design machines that automate a series of processes from purification of samples to analysis.”
Reference
Thursday, July 12, 2007
IMMUNOLOGY:Arresting autoimmunity
Working with a mouse version of multiple sclerosis, Gang Pei and colleagues study a protein called beta-arrestin 1, a factor known to regulate gene expression in all cells. Pei’s team reports that beta-arrestin 1 helps promote survival of T lymphocytes, which increases the duration of inflammation. In the absence of beta-arrestin 1 a critical factor required for T lymphocyte survival is not produced. Consistently, T lymphocytes lacking beta-arrestin 1 survive less well and cause much less brain inflammation in a mouse model of multiple sclerosis.
Demonstrating a role for beta-arrestin 1 in prolonging survival of aggressive T lymphocytes associated with autoimmune disease provides a possible target for reducing such diseases. Whether blocking the function of beta-arrestin 1 will help multiple sclerosis patients, however, remains a question for future investigation.
Author contact:
Gang Pei (Shanghai Institutes for Biological Sciences, China)
Tel: +86 21 5492 1371; E-mail: gpei@sibs.ac.cn
Working with a mouse version of multiple sclerosis, Gang Pei and colleagues study a protein called beta-arrestin 1, a factor known to regulate gene expression in all cells. Pei’s team reports that beta-arrestin 1 helps promote survival of T lymphocytes, which increases the duration of inflammation. In the absence of beta-arrestin 1 a critical factor required for T lymphocyte survival is not produced. Consistently, T lymphocytes lacking beta-arrestin 1 survive less well and cause much less brain inflammation in a mouse model of multiple sclerosis.
Demonstrating a role for beta-arrestin 1 in prolonging survival of aggressive T lymphocytes associated with autoimmune disease provides a possible target for reducing such diseases. Whether blocking the function of beta-arrestin 1 will help multiple sclerosis patients, however, remains a question for future investigation.
Author contact:
Gang Pei (Shanghai Institutes for Biological Sciences, China)
Tel: +86 21 5492 1371; E-mail: gpei@sibs.ac.cn
Growth factor reinforces cocaine addiction
Release of a growth factor in the nucleus accumbens – a brain area mediating reward – is necessary for the development and relapse of cocaine addiction.
Addictive drugs are thought to ‘hijack’ reward systems in the brain, causing neurons to be persistently more responsive to drug-associated cues and stressors. David Self and colleagues report that four hours after cocaine self-administration, rats show an increase in brain-derived neurotrophic factor (BDNF) in the nucleus accumbens. Preventing this increase in BDNF reduced cocaine self-administration and the propensity to relapse, whereas giving the rats daily BDNF injections after cocaine self-administration increased cocaine-seeking behaviour and relapse.
Moreover, using mice that were genetically engineered to lack BDNF only in the nucleus accumbens in adulthood, they showed that BDNF release in the nucleus accumbens did not affect the initial rewarding effects of cocaine, but did dramatically alter the development of addiction. If similar mechanisms mediate addiction in humans, these results could suggest possible approaches to addiction treatment.
Author contact:
David Self (University of Texas Southwestern Medical Center, Dallas, TX, USA)
Tel: +1 214 648 1237; E-mail: david.self@utsouthwestern.edu
Release of a growth factor in the nucleus accumbens – a brain area mediating reward – is necessary for the development and relapse of cocaine addiction.
Addictive drugs are thought to ‘hijack’ reward systems in the brain, causing neurons to be persistently more responsive to drug-associated cues and stressors. David Self and colleagues report that four hours after cocaine self-administration, rats show an increase in brain-derived neurotrophic factor (BDNF) in the nucleus accumbens. Preventing this increase in BDNF reduced cocaine self-administration and the propensity to relapse, whereas giving the rats daily BDNF injections after cocaine self-administration increased cocaine-seeking behaviour and relapse.
Moreover, using mice that were genetically engineered to lack BDNF only in the nucleus accumbens in adulthood, they showed that BDNF release in the nucleus accumbens did not affect the initial rewarding effects of cocaine, but did dramatically alter the development of addiction. If similar mechanisms mediate addiction in humans, these results could suggest possible approaches to addiction treatment.
Author contact:
David Self (University of Texas Southwestern Medical Center, Dallas, TX, USA)
Tel: +1 214 648 1237; E-mail: david.self@utsouthwestern.edu
Common genetic risk variant for colorectal cancer
A common variant on chromosome 8 that predisposes to prostate cancer also confers risk of colorectal cancer, according to three studies.Although a few relatively rare mutations have been identified that are associated with colorectal cancer, this is the first evidence for a common genetic risk factor. Colorectal cancer is one of the most commonly diagnosed forms of cancer.
In the first study, Richard Houlston, Ian Tomlinson and colleagues carried out a genome-wide association study for colorectal cancer and identified the most strongly associated variant on chromosome 8 as the same variant that had previously been associated with risk of prostate cancer. In the second study, Thomas Hudson, Malcolm Dunlop and colleagues screened a smaller number of variants across the genome but identified the same one on chromosome 8 as highly associated with colorectal cancer. Finally, Christopher Haiman and colleagues noted that the region on chromosome 8 that was shown to be associated with prostate cancer is also known to be amplified in individuals with colorectal cancer. Given this background they directly assessed the relevant variants in individuals with colorectal cancer and found them to be significantly more frequent than in cancer-free individuals. Haiman and colleagues also note that five other variants in this region that had been associated with prostate cancer were not associated with colorectal cancer, suggesting that the mechanism by which variants in the region contribute to cancer risk may differ depending on the type of cancer.
Author contacts:
Richard Houlston (Institute of Cancer Research, Sutton, UK)
Tel: +44 208 722 4175; E-mail: richard.houlston@icr.ac.uk
Ian Tomlinson (London Research Institute, Cancer Research UK)
Tel: +44 207 269 2884; E-mail: ian.tomlinson@cancer.org.uk Authors paper [7]
Thomas Hudson (The Ontario Institute for Cancer Research, Toronto, Ontario, Canada)
Tel: +1 416 673 6650; E-mail: tom.hudson@oicr.on.ca
Malcolm Dunlop (University of Edinburgh, UK)
Tel: +44 131 467 8439; E-mail: malcolm.dunlop@hgu.mrc.ac.uk Authors paper [8]
Christopher Haiman (University of Southern California, Los Angeles, CA, USA)
Tel: +1 323 865 0429; E-mail: haiman@usc.edu Author paper [9]
A common variant on chromosome 8 that predisposes to prostate cancer also confers risk of colorectal cancer, according to three studies.Although a few relatively rare mutations have been identified that are associated with colorectal cancer, this is the first evidence for a common genetic risk factor. Colorectal cancer is one of the most commonly diagnosed forms of cancer.
In the first study, Richard Houlston, Ian Tomlinson and colleagues carried out a genome-wide association study for colorectal cancer and identified the most strongly associated variant on chromosome 8 as the same variant that had previously been associated with risk of prostate cancer. In the second study, Thomas Hudson, Malcolm Dunlop and colleagues screened a smaller number of variants across the genome but identified the same one on chromosome 8 as highly associated with colorectal cancer. Finally, Christopher Haiman and colleagues noted that the region on chromosome 8 that was shown to be associated with prostate cancer is also known to be amplified in individuals with colorectal cancer. Given this background they directly assessed the relevant variants in individuals with colorectal cancer and found them to be significantly more frequent than in cancer-free individuals. Haiman and colleagues also note that five other variants in this region that had been associated with prostate cancer were not associated with colorectal cancer, suggesting that the mechanism by which variants in the region contribute to cancer risk may differ depending on the type of cancer.
Author contacts:
Richard Houlston (Institute of Cancer Research, Sutton, UK)
Tel: +44 208 722 4175; E-mail: richard.houlston@icr.ac.uk
Ian Tomlinson (London Research Institute, Cancer Research UK)
Tel: +44 207 269 2884; E-mail: ian.tomlinson@cancer.org.uk Authors paper [7]
Thomas Hudson (The Ontario Institute for Cancer Research, Toronto, Ontario, Canada)
Tel: +1 416 673 6650; E-mail: tom.hudson@oicr.on.ca
Malcolm Dunlop (University of Edinburgh, UK)
Tel: +44 131 467 8439; E-mail: malcolm.dunlop@hgu.mrc.ac.uk Authors paper [8]
Christopher Haiman (University of Southern California, Los Angeles, CA, USA)
Tel: +1 323 865 0429; E-mail: haiman@usc.edu Author paper [9]
Nanocrystal shape control
The shape of metal nanocrystals can be accurately controlled by using a small particle of a different metal as a seed.
Peidong Yang and co-authors reacted a platinum nanocube (~13 nanometres each side) with a palladium-based compound to produce core–shell Pt/Pd nanocrystals. By varying the reaction environment, and in particular the amount of NO2, the researchers were able to obtain three different shapes — cubes, cuboctahedra and octahedra.
Many of the physical and chemical properties of nanocrystals depend strongly on their morphology. The authors show, for example, that the catalytic activity of the cubes is quite different from that of the other two types of nanocrystals. The use of seeds represents a clear step towards the development of nanocrystals with well-defined shapes.
Author contact:
Peidong Yang (University of California, Berkley, CA, USA)
Tel: +1 510 643 1545; E-mail: p_yang@berkeley.edu
The shape of metal nanocrystals can be accurately controlled by using a small particle of a different metal as a seed.
Peidong Yang and co-authors reacted a platinum nanocube (~13 nanometres each side) with a palladium-based compound to produce core–shell Pt/Pd nanocrystals. By varying the reaction environment, and in particular the amount of NO2, the researchers were able to obtain three different shapes — cubes, cuboctahedra and octahedra.
Many of the physical and chemical properties of nanocrystals depend strongly on their morphology. The authors show, for example, that the catalytic activity of the cubes is quite different from that of the other two types of nanocrystals. The use of seeds represents a clear step towards the development of nanocrystals with well-defined shapes.
Author contact:
Peidong Yang (University of California, Berkley, CA, USA)
Tel: +1 510 643 1545; E-mail: p_yang@berkeley.edu
new method to detect small changes in human genes
A new method to detect small changes in human genes could lead the way in personalized medicine. The most common type of variation in our genes is a single difference in one of the nucleotide building blocks of the DNA sequence, known as single nucleotide polymorphism (SNP—pronounced ‘snip’). Scientists believe differences in SNPs reveal an individual’s susceptibility to disease, meaning accurate analysis of SNPs would play a key role in diagnostics. These small SNP variations can account for as little as 0.1 per cent of a genome sequence.
SNP diagnostics have recently attracted much attention and several strategies to identify SNPs have been developed in the past few years. Existing methods are often limited by the need to identify large DNA sequences. Now, a team of Japanese researchers led by Akimitsu Okamoto from the RIKEN Frontier Research System, Wako, has used derivatives of the fluorescent dye PRODAN to correctly identify SNPs quickly and efficiently1.
PRODAN, a well-known fluorophore, absorbs and emits light at different wavelengths depending on the polarity of its environment. Okamoto reasoned that similar dyes, which include differing nucleotide components, could be incorporated into DNA structures and ‘report back’ differences in the microenvironment. Such changes in the microenvironment would likely be the result of small changes in the DNA structure and allow detection of sequence variations (Fig. 1 - Click on link below). The team synthesized four variants of the dye, so that all combinations of base matches and mismatches could be investigated.
Once incorporated in a DNA sequence under a variety of conditions, the team calculated the differences between the wavelengths absorbed and emitted by the dye. These differences are known as Stokes shifts. The researchers detected a small Stokes shift when DNA base pairs matched correctly, but a larger shift when there was a mismatch. Therefore, by using various PRODAN-labeled DNA dyes, single nucleotide alterations could be detected. “The use of this DNA probe makes it possible to judge the type of base located at a specific site on the target DNA, simply by mixing the DNA and the dye together. This method is a very powerful assay that does not require enzymes or time-consuming steps, and avoids errors,” says Okamoto.
Okamoto believes that this method of detection is very promising and is working towards making the system suitable for every day use. “I think SNP chips using our probe would make important contributions to cancer diagnosis,” he enthuses.
A new method to detect small changes in human genes could lead the way in personalized medicine. The most common type of variation in our genes is a single difference in one of the nucleotide building blocks of the DNA sequence, known as single nucleotide polymorphism (SNP—pronounced ‘snip’). Scientists believe differences in SNPs reveal an individual’s susceptibility to disease, meaning accurate analysis of SNPs would play a key role in diagnostics. These small SNP variations can account for as little as 0.1 per cent of a genome sequence.
SNP diagnostics have recently attracted much attention and several strategies to identify SNPs have been developed in the past few years. Existing methods are often limited by the need to identify large DNA sequences. Now, a team of Japanese researchers led by Akimitsu Okamoto from the RIKEN Frontier Research System, Wako, has used derivatives of the fluorescent dye PRODAN to correctly identify SNPs quickly and efficiently1.
PRODAN, a well-known fluorophore, absorbs and emits light at different wavelengths depending on the polarity of its environment. Okamoto reasoned that similar dyes, which include differing nucleotide components, could be incorporated into DNA structures and ‘report back’ differences in the microenvironment. Such changes in the microenvironment would likely be the result of small changes in the DNA structure and allow detection of sequence variations (Fig. 1 - Click on link below). The team synthesized four variants of the dye, so that all combinations of base matches and mismatches could be investigated.
Once incorporated in a DNA sequence under a variety of conditions, the team calculated the differences between the wavelengths absorbed and emitted by the dye. These differences are known as Stokes shifts. The researchers detected a small Stokes shift when DNA base pairs matched correctly, but a larger shift when there was a mismatch. Therefore, by using various PRODAN-labeled DNA dyes, single nucleotide alterations could be detected. “The use of this DNA probe makes it possible to judge the type of base located at a specific site on the target DNA, simply by mixing the DNA and the dye together. This method is a very powerful assay that does not require enzymes or time-consuming steps, and avoids errors,” says Okamoto.
Okamoto believes that this method of detection is very promising and is working towards making the system suitable for every day use. “I think SNP chips using our probe would make important contributions to cancer diagnosis,” he enthuses.
Origin of adult blood cells clarified
A research team at the RIKEN Center for Developmental Biology, Kobe, has developed a cell tracing method that unambiguously identifies the yolk sac—an extra-embryonic structure—as a source of blood cells in both the embryo and, later, the adult.
Developmental biologists have debated the original source blood cells in adult mammals for over thirty years. Now, a team led by Igor Samokhvalov at the RIKEN Center for Developmental Biology, Kobe, has developed a cell tracing method that unambiguously identifies the yolk sac—an extra-embryonic structure—as a source of blood cells in both the embryo and, later, the adult.
The yolk sac, which provides the developing embryo with nutrients, is the first extra-embryonic structure to form during embryogenesis. This structure is also the first place of embryonic blood cell formation (hematopoiesis). A central question in developmental biology about hematopoiesis is the role—if any—the yolk sac-derived blood cells play in the development of adult blood cells.
“The origin of [the] hematopoietic [blood] system was always obscure and controversial; this was the reason I became interested in this area of hematology,” says Samokhvalov.
To resolve the controversy, the team labored for two years to develop a cell tracing method to follow yolk sac-derived blood cells through later stages of embryonic development1. The ability to study this development non-invasively through time was critical, says Samokhvalov, because removing cells from tissue introduces stresses that can lead to an inaccurate picture of actual embryonic processes.
The method consists of replacing of one copy of a gene called Runx1, which is essential for blood development, with another gene that produces a protein creating ‘tags’ in the cells and all their progeny. The ‘new’ gene is turned on at the same time Runx1 normally is—at a mere 7.5 days after embryonic development begins.
Tagging the earliest Runx1-expressing yolk sac cells at day 7.5 of development allowed the team to follow these cells’ progeny when they’re incorporated into blood vessel walls (Fig. 1 - Click on link below), and evaluate their long-term contribution to the adult blood system.
So clear were the results, remarks Samokhvalov, that “our work showed direct contribution of [the] yolk sac to adult haematopoiesis”. Indeed, the team’s direct and carefully designed cell tracing methodology eliminated ambiguities that could lead to alternative interpretations.
This work settles the long-standing controversy, marking an important step forward in developmental biology. However, the team’s data do not rule out the possibility of an additional source of haematopoietic stem cells in the embryo.
Samokhvalov’s future plans include determining more precisely the extent of the yolk sac’s participation in adult blood development, and whether another source of haematopoietic stem cells occurs in the embryo itself.
A research team at the RIKEN Center for Developmental Biology, Kobe, has developed a cell tracing method that unambiguously identifies the yolk sac—an extra-embryonic structure—as a source of blood cells in both the embryo and, later, the adult.
Developmental biologists have debated the original source blood cells in adult mammals for over thirty years. Now, a team led by Igor Samokhvalov at the RIKEN Center for Developmental Biology, Kobe, has developed a cell tracing method that unambiguously identifies the yolk sac—an extra-embryonic structure—as a source of blood cells in both the embryo and, later, the adult.
The yolk sac, which provides the developing embryo with nutrients, is the first extra-embryonic structure to form during embryogenesis. This structure is also the first place of embryonic blood cell formation (hematopoiesis). A central question in developmental biology about hematopoiesis is the role—if any—the yolk sac-derived blood cells play in the development of adult blood cells.
“The origin of [the] hematopoietic [blood] system was always obscure and controversial; this was the reason I became interested in this area of hematology,” says Samokhvalov.
To resolve the controversy, the team labored for two years to develop a cell tracing method to follow yolk sac-derived blood cells through later stages of embryonic development1. The ability to study this development non-invasively through time was critical, says Samokhvalov, because removing cells from tissue introduces stresses that can lead to an inaccurate picture of actual embryonic processes.
The method consists of replacing of one copy of a gene called Runx1, which is essential for blood development, with another gene that produces a protein creating ‘tags’ in the cells and all their progeny. The ‘new’ gene is turned on at the same time Runx1 normally is—at a mere 7.5 days after embryonic development begins.
Tagging the earliest Runx1-expressing yolk sac cells at day 7.5 of development allowed the team to follow these cells’ progeny when they’re incorporated into blood vessel walls (Fig. 1 - Click on link below), and evaluate their long-term contribution to the adult blood system.
So clear were the results, remarks Samokhvalov, that “our work showed direct contribution of [the] yolk sac to adult haematopoiesis”. Indeed, the team’s direct and carefully designed cell tracing methodology eliminated ambiguities that could lead to alternative interpretations.
This work settles the long-standing controversy, marking an important step forward in developmental biology. However, the team’s data do not rule out the possibility of an additional source of haematopoietic stem cells in the embryo.
Samokhvalov’s future plans include determining more precisely the extent of the yolk sac’s participation in adult blood development, and whether another source of haematopoietic stem cells occurs in the embryo itself.
It’s all in the Electron Spin
Japanese researchers show subtle fluctuations in electron spins are the origin of magnetism and superconductivity in a common oxide
Magnetism and superconductivity are material properties that generally exclude each other. The reason is that in a magnet, the electron spins—tiny magnets responsible for the material’s magnetism—align in a common direction. On the other hand, superconductivity requires the pairing of electrons with opposing spins.
In that respect, sodium cobalt oxide, NaxCoO2, is unusual. It has a lattice structure with crystal planes formed by cobalt (Co) and oxygen (O) atoms. Along those planes it is ferromagnetic. However, when brought into contact with water, water molecules integrate into the material’s crystal structure forming a slightly modified hydrated compound, NaxCoO2 • yH2O. And, this compound shows superconductivity along the CoO2 planes at low temperatures.
However, a team of researchers from RIKEN’s Discovery Research Institute in Wako, and colleagues from the universities of Chofu and Nagoya, now propose that magnetism and superconductivity in the non-hydrated and hydrated forms of NaxCoO2 actually share a common origin (1).
Typically, the origin of properties such as magnetism or superconductivity lies in the way electrons occupy the internal electronic states of a material. Like water filling an empty bucket, electrons in a material occupy all available electronic states beginning with the ones having the lowest electronic energy. Those electrons ending up at the ‘top’ of the bucket, also called the ‘Fermi surface’ (Fig. 1 - click on link below), are responsible for the electronic behavior of a material.
This Fermi surface can take quite complicated shapes. It can even consist of completely separate regions, particularly in crystals that are not symmetric in all directions. This is the case for NaxCoO2.
The researchers studied the theoretical electron interaction between the disconnected parts of the Fermi surface and found that electrons can jump between these ‘islands’. This is made possible by so-called ‘spin fluctuations’—tiny changes in the way electron spins are aligned with each other. Through these synchronized tilts in their spins, electrons can gather just the right amount of energy to bridge the gaps at the Fermi surface. This electron interaction is crucial to mediate the material’s electronic properties and, according to Ryotaro Arita from the RIKEN team, “provides the necessary incentive for the electrons to create either ferromagnetism or superconductivity”.
Such a common origin for both phenomena in NaxCoO2 is quite rare, although Arita is convinced that if proven experimentally, this might lead to the discovery of other superconducting materials with disconnected Fermi surfaces.
Reference
1. Kuroki, K., Ohkubo, S., Nojima, T., Arita, R., Onari, S. & Tanaka, Y. Unified origin for the 3D magnetism and superconductivity in NaxCoO2. Physical Review Letters 98, 136401 (2007).
For more information, contact
Saeko Okada
Email: okadas@riken.jp
Japanese researchers show subtle fluctuations in electron spins are the origin of magnetism and superconductivity in a common oxide
Magnetism and superconductivity are material properties that generally exclude each other. The reason is that in a magnet, the electron spins—tiny magnets responsible for the material’s magnetism—align in a common direction. On the other hand, superconductivity requires the pairing of electrons with opposing spins.
In that respect, sodium cobalt oxide, NaxCoO2, is unusual. It has a lattice structure with crystal planes formed by cobalt (Co) and oxygen (O) atoms. Along those planes it is ferromagnetic. However, when brought into contact with water, water molecules integrate into the material’s crystal structure forming a slightly modified hydrated compound, NaxCoO2 • yH2O. And, this compound shows superconductivity along the CoO2 planes at low temperatures.
However, a team of researchers from RIKEN’s Discovery Research Institute in Wako, and colleagues from the universities of Chofu and Nagoya, now propose that magnetism and superconductivity in the non-hydrated and hydrated forms of NaxCoO2 actually share a common origin (1).
Typically, the origin of properties such as magnetism or superconductivity lies in the way electrons occupy the internal electronic states of a material. Like water filling an empty bucket, electrons in a material occupy all available electronic states beginning with the ones having the lowest electronic energy. Those electrons ending up at the ‘top’ of the bucket, also called the ‘Fermi surface’ (Fig. 1 - click on link below), are responsible for the electronic behavior of a material.
This Fermi surface can take quite complicated shapes. It can even consist of completely separate regions, particularly in crystals that are not symmetric in all directions. This is the case for NaxCoO2.
The researchers studied the theoretical electron interaction between the disconnected parts of the Fermi surface and found that electrons can jump between these ‘islands’. This is made possible by so-called ‘spin fluctuations’—tiny changes in the way electron spins are aligned with each other. Through these synchronized tilts in their spins, electrons can gather just the right amount of energy to bridge the gaps at the Fermi surface. This electron interaction is crucial to mediate the material’s electronic properties and, according to Ryotaro Arita from the RIKEN team, “provides the necessary incentive for the electrons to create either ferromagnetism or superconductivity”.
Such a common origin for both phenomena in NaxCoO2 is quite rare, although Arita is convinced that if proven experimentally, this might lead to the discovery of other superconducting materials with disconnected Fermi surfaces.
Reference
1. Kuroki, K., Ohkubo, S., Nojima, T., Arita, R., Onari, S. & Tanaka, Y. Unified origin for the 3D magnetism and superconductivity in NaxCoO2. Physical Review Letters 98, 136401 (2007).
For more information, contact
Saeko Okada
Email: okadas@riken.jp
Tuesday, July 03, 2007
Adult Stem Cells Show Promise for Peripheral Vascular Disease
Adult stem cells cultivated from patients' own blood can potentially improve the quality of life for patients whose lower extremities are affected by peripheral vascular disease, according to a study in China.
SHENZHEN, China, July 3, 2007 (medianowonline)-Beike Biotechnology Co., Ltd. today announced that a team led by Dr. Yang Xiaofeng at its collaborating hospital in Shenyang completed a study to assess clinical efficacy, safety, and feasibility of transplantation of peripheral blood stem cells for patients with peripheral vascular disease of the lower extremities.
Beike is best known for its research and treatments for ataxia, cerebral palsy, spinal cord injury and MS which are often covered by China Stem Cell News.However, Beike also has broad experience in research and treating vascular diseases with adult stem cells mostly through its collaboration with Shenyang 463 hospital.
A total of 152 patients with peripheral vascular disease of the lower extremities were enrolled into this non-controlled study from November 2003 to March 2006. The results were published in the Journal of Geriatric Cardiology which publishes original peer-reviewed clinical and experimental reports on all aspects of cardiovascular disease in the elderly.
A second study was completed during the same period comparing the relative improvement of lower limb ischemia (lack of blood supply) between transplantation of autologous peripheral blood stem cells and transplantation of bone marrow stem cells. The study is awaiting publication in a peer-reviewed journal.
At 12 weeks, primary symptoms, including lower limb pain and coldness, were significantly improved in 137 (90.1%) of the patients; limb ulcers improved or healed in 46 (86.8%) of the 53 patients, while 25 of the 48 (47.9%) patients with limb gangrene remained steady or improved. Angiography (an X-ray) before treatment, and at 12 weeks after treatment, was performed in 10 of the patients and showed formation of new collateral vessels.
The patients had no severe adverse effects or complications related to cell transplantation.
"These preliminary results, while encouraging, must be further researched in future controlled studies and reinforced by separate studies by other laboratories," said Yang Xiao Feng, Director of the Stem Cell Program for Vascular Diseases at Shenyang 463 Hospital.
The study followed previous studies done in the laboratory and pre-clinical work done in rabbits.
"There is evidence demonstrating significant improvement in the quality of life of patients receiving the treatment, including formation of new collateral vessels," said Sean Hu, Chairman of Beike Biotechnology group. "We are now working to collaborate with institutions in the U.S. to further substantiate this and other studies including those we are doing for neurological diseases using umbilical cord stem cells."
In 2006, Beike Biotechnology completed two studies involving eight patients with ALS. Two papers were published in the Journal of Zhenghou University of Medical Science. The first observed the effect of transplantation of umbilical cord blood mesenchymal stem cells (UCB-MSCs) on glutamate (Glu) levels in plasma and CSF of amyotrophic lateral sclerosis patients and the second observed the effect of umbilical cord blood mesenchymal stem cell transplantation on nervous system function of ALS patients.
The abstract of this study on treatment of peripheral vascular disease can be found at: http://www.jgeriatriccard.com/id10abstract-september06.html.
Adult stem cells cultivated from patients' own blood can potentially improve the quality of life for patients whose lower extremities are affected by peripheral vascular disease, according to a study in China.
SHENZHEN, China, July 3, 2007 (medianowonline)-Beike Biotechnology Co., Ltd. today announced that a team led by Dr. Yang Xiaofeng at its collaborating hospital in Shenyang completed a study to assess clinical efficacy, safety, and feasibility of transplantation of peripheral blood stem cells for patients with peripheral vascular disease of the lower extremities.
Beike is best known for its research and treatments for ataxia, cerebral palsy, spinal cord injury and MS which are often covered by China Stem Cell News.However, Beike also has broad experience in research and treating vascular diseases with adult stem cells mostly through its collaboration with Shenyang 463 hospital.
A total of 152 patients with peripheral vascular disease of the lower extremities were enrolled into this non-controlled study from November 2003 to March 2006. The results were published in the Journal of Geriatric Cardiology which publishes original peer-reviewed clinical and experimental reports on all aspects of cardiovascular disease in the elderly.
A second study was completed during the same period comparing the relative improvement of lower limb ischemia (lack of blood supply) between transplantation of autologous peripheral blood stem cells and transplantation of bone marrow stem cells. The study is awaiting publication in a peer-reviewed journal.
At 12 weeks, primary symptoms, including lower limb pain and coldness, were significantly improved in 137 (90.1%) of the patients; limb ulcers improved or healed in 46 (86.8%) of the 53 patients, while 25 of the 48 (47.9%) patients with limb gangrene remained steady or improved. Angiography (an X-ray) before treatment, and at 12 weeks after treatment, was performed in 10 of the patients and showed formation of new collateral vessels.
The patients had no severe adverse effects or complications related to cell transplantation.
"These preliminary results, while encouraging, must be further researched in future controlled studies and reinforced by separate studies by other laboratories," said Yang Xiao Feng, Director of the Stem Cell Program for Vascular Diseases at Shenyang 463 Hospital.
The study followed previous studies done in the laboratory and pre-clinical work done in rabbits.
"There is evidence demonstrating significant improvement in the quality of life of patients receiving the treatment, including formation of new collateral vessels," said Sean Hu, Chairman of Beike Biotechnology group. "We are now working to collaborate with institutions in the U.S. to further substantiate this and other studies including those we are doing for neurological diseases using umbilical cord stem cells."
In 2006, Beike Biotechnology completed two studies involving eight patients with ALS. Two papers were published in the Journal of Zhenghou University of Medical Science. The first observed the effect of transplantation of umbilical cord blood mesenchymal stem cells (UCB-MSCs) on glutamate (Glu) levels in plasma and CSF of amyotrophic lateral sclerosis patients and the second observed the effect of umbilical cord blood mesenchymal stem cell transplantation on nervous system function of ALS patients.
The abstract of this study on treatment of peripheral vascular disease can be found at: http://www.jgeriatriccard.com/id10abstract-september06.html.
Monday, July 02, 2007
Fight against Cancer
UPM scientists are researching the possibility of using "tapai ubi", or fermented tapioca, as a prevention against cancer. Preliminary tests indicated that seven types of cancer, including cervical, ovarian, breast and leukaemia, could be prevented by eating tapai ubi.
Researchers: Latifah Saiful Yazan, Foo Hooi Ling, Raha Abdul Rahim and Loh Teck Chwen
UPM scientists are researching the possibility of using tapai ubi, or fermented tapioca, as a prevention against cancer. Lactobacillus plantarum UL4 (Lactic Acid Bacteria) isolated from local tapai ubi (fermented tapioca, Manihot esculanta ) is able to produce bacteriocin (designated as bacteriocin UL4) that shows broad inhibitory activities towards a numbers of pathogens, such as Bacillus cereus, Escherichia coli, Streptococcus pneumoniae, Staphylococcus aureus, Salmonella typhimurium, Enterococcus faecium and Listeria monocytogenes. Bacteriocin UL4 not only can withstand high temperatures up to 121ºC for 15 minutes but is also stable at temperatures below 15ºC for up to 60 days.
As for pH tolerence, the bacteriocin UL4 is also tolerable to broad pH range, which includes acidic (pH 2-5) and basic (pH 7-8) pH. The physiological effects of bacteriocin UL4 have been studied by feeding to post weaning rats as feed additive.
The feeding trial results demonstrated that it could reduce the total plasma cholesterol concentration and the Enterobacteriaceae counts significantly as compared to the control group. Under the study conducted at UPM, the bacterioicn UL4 also exhibited positive in vitro cytotoxic activities towards a few cancerous cell lines, for instances breast carcinoma (estrogen receptor-positive MCF7 and estrogen receptor-negative MDA MB231), cervical adenocarcinoma (HeLa), ovarian cancer (CaOV3) and acute promyelocytic leukaemia (HL60) cells.
However no detailed study has been carried out yet to evaluate the cancer chemopreventive activities of bacteriocin. By knowing the potential of the bacteriocin to fight various malignancies, this work is proposed to assess its anti-tumour promoting activity on mice induced with skin cancer. Our preliminary tests indicated that seven types of cancer, including cervical, ovarian, breast and leukaemia, could be prevented by eating tapai ubi.
UPM scientists are researching the possibility of using "tapai ubi", or fermented tapioca, as a prevention against cancer. Preliminary tests indicated that seven types of cancer, including cervical, ovarian, breast and leukaemia, could be prevented by eating tapai ubi.
Researchers: Latifah Saiful Yazan, Foo Hooi Ling, Raha Abdul Rahim and Loh Teck Chwen
UPM scientists are researching the possibility of using tapai ubi, or fermented tapioca, as a prevention against cancer. Lactobacillus plantarum UL4 (Lactic Acid Bacteria) isolated from local tapai ubi (fermented tapioca, Manihot esculanta ) is able to produce bacteriocin (designated as bacteriocin UL4) that shows broad inhibitory activities towards a numbers of pathogens, such as Bacillus cereus, Escherichia coli, Streptococcus pneumoniae, Staphylococcus aureus, Salmonella typhimurium, Enterococcus faecium and Listeria monocytogenes. Bacteriocin UL4 not only can withstand high temperatures up to 121ºC for 15 minutes but is also stable at temperatures below 15ºC for up to 60 days.
As for pH tolerence, the bacteriocin UL4 is also tolerable to broad pH range, which includes acidic (pH 2-5) and basic (pH 7-8) pH. The physiological effects of bacteriocin UL4 have been studied by feeding to post weaning rats as feed additive.
The feeding trial results demonstrated that it could reduce the total plasma cholesterol concentration and the Enterobacteriaceae counts significantly as compared to the control group. Under the study conducted at UPM, the bacterioicn UL4 also exhibited positive in vitro cytotoxic activities towards a few cancerous cell lines, for instances breast carcinoma (estrogen receptor-positive MCF7 and estrogen receptor-negative MDA MB231), cervical adenocarcinoma (HeLa), ovarian cancer (CaOV3) and acute promyelocytic leukaemia (HL60) cells.
However no detailed study has been carried out yet to evaluate the cancer chemopreventive activities of bacteriocin. By knowing the potential of the bacteriocin to fight various malignancies, this work is proposed to assess its anti-tumour promoting activity on mice induced with skin cancer. Our preliminary tests indicated that seven types of cancer, including cervical, ovarian, breast and leukaemia, could be prevented by eating tapai ubi.
Sunday, July 01, 2007
Fishy genome swims into view
The medaka fish (Oryzias latipes), a popular pet in Japan and model organism in the laboratory, has had its genome sequenced.
Shinichi Morishita and colleagues estimate that the small egg-laying freshwater fish’s genome contains approximately 20,000 genes, of which around 2,900 appear new and unique to medaka.
Teleosts (fish with bony skeletons), such as the medaka fish, make up more than half of all vertebrate species and have adapted to life in a variety of marine and freshwater habitats. The evolution and diversification of their genomes is therefore crucial to understanding how vertebrates evolved.
The team compared their high-quality draft sequence against human, pufferfish (Tetraodon) and zebrafish genomes. It’s already known that at some point in the past the whole teleost genome doubled. The new study shows that the last common ancestor of medaka, pufferfish and zebrafish experienced 8 major rearrangements between chromosomes within just 50 million years of this event. But where the zebrafish genome has changed considerably since it diverged from the last common ancestor some 320 million years ago, the medaka genome has remained remarkably unchanged for over 300 million years.
CONTACT
Shinichi Morishita (University of Tokyo, Chiba, Japan)
Tel: +81 47 136 3984; E-mail: moris@cb.k.u-tokyo.ac.jp
The medaka fish (Oryzias latipes), a popular pet in Japan and model organism in the laboratory, has had its genome sequenced.
Shinichi Morishita and colleagues estimate that the small egg-laying freshwater fish’s genome contains approximately 20,000 genes, of which around 2,900 appear new and unique to medaka.
Teleosts (fish with bony skeletons), such as the medaka fish, make up more than half of all vertebrate species and have adapted to life in a variety of marine and freshwater habitats. The evolution and diversification of their genomes is therefore crucial to understanding how vertebrates evolved.
The team compared their high-quality draft sequence against human, pufferfish (Tetraodon) and zebrafish genomes. It’s already known that at some point in the past the whole teleost genome doubled. The new study shows that the last common ancestor of medaka, pufferfish and zebrafish experienced 8 major rearrangements between chromosomes within just 50 million years of this event. But where the zebrafish genome has changed considerably since it diverged from the last common ancestor some 320 million years ago, the medaka genome has remained remarkably unchanged for over 300 million years.
CONTACT
Shinichi Morishita (University of Tokyo, Chiba, Japan)
Tel: +81 47 136 3984; E-mail: moris@cb.k.u-tokyo.ac.jp
Hurricanes: Back to normal?
The increase in the number of major Atlantic hurricanes since 1995 could be a recovery to normal activity, rather than a rise to unusually high levels. According to the study, which uses proxy records of vertical wind shear and sea surface temperature to reconstruct the number of major Atlantic hurricanes over the past 270 years, the storm frequency was anomalously low during the 1970s and 1980s.
The frequency of major hurricanes over the Atlantic Ocean has risen significantly since 1995, but it remains unclear whether this change is due to global warming or natural variability. One way to address this question is to consider changes in hurricane activity in the past, but reliable observations only cover the past few decades.
Johan Nyberg and colleagues used proxy records from corals and a marine sediment core that reflect changes in the two main parameters that influence hurricane activity — vertical wind shear and sea surface temperature — to reconstruct the frequency of major hurricanes over the Atlantic since 1730. The records show that the lull in hurricane activity from the late 1960s to early 1990s is an exception, and that the current active period from 1995 onwards reflects a return to ‘normal’ activity, rather than a direct response to increasing sea surface temperature. The records indicate that variations in vertical wind shear may have been responsible for the changes in hurricane frequency, although the underlying causes of changes in this parameter remain uncertain. The authors suggest that it is therefore crucial to understand future changes in the magnitude of vertical wind shear, because they may have a significant influence on hurricane activity.
CONTACT
Johan Nyberg (Geological Survey of Sweden, Uppsala, Sweden)
Tel: +46 18 17 91 94; E-mail: johan.nyberg@sgu.se
James B. Elsner (Florida State University, Tallahassee, FL, USA) N&V author
Tel: +1 850 877 4039; E-mail: jelsner@fsu.edu
The increase in the number of major Atlantic hurricanes since 1995 could be a recovery to normal activity, rather than a rise to unusually high levels. According to the study, which uses proxy records of vertical wind shear and sea surface temperature to reconstruct the number of major Atlantic hurricanes over the past 270 years, the storm frequency was anomalously low during the 1970s and 1980s.
The frequency of major hurricanes over the Atlantic Ocean has risen significantly since 1995, but it remains unclear whether this change is due to global warming or natural variability. One way to address this question is to consider changes in hurricane activity in the past, but reliable observations only cover the past few decades.
Johan Nyberg and colleagues used proxy records from corals and a marine sediment core that reflect changes in the two main parameters that influence hurricane activity — vertical wind shear and sea surface temperature — to reconstruct the frequency of major hurricanes over the Atlantic since 1730. The records show that the lull in hurricane activity from the late 1960s to early 1990s is an exception, and that the current active period from 1995 onwards reflects a return to ‘normal’ activity, rather than a direct response to increasing sea surface temperature. The records indicate that variations in vertical wind shear may have been responsible for the changes in hurricane frequency, although the underlying causes of changes in this parameter remain uncertain. The authors suggest that it is therefore crucial to understand future changes in the magnitude of vertical wind shear, because they may have a significant influence on hurricane activity.
CONTACT
Johan Nyberg (Geological Survey of Sweden, Uppsala, Sweden)
Tel: +46 18 17 91 94; E-mail: johan.nyberg@sgu.se
James B. Elsner (Florida State University, Tallahassee, FL, USA) N&V author
Tel: +1 850 877 4039; E-mail: jelsner@fsu.edu
Oncology: MicroRNAs and tumour suppression
The tumour suppressor p53 acts directly on a family of small RNAs that are vital for cell growth and replication. Already well known for its indirect effects, p53 is now shown to target the miR-34 family of microRNAs (miRNAs), which itself suppresses cell proliferation.
A global decrease in miRNA levels is often observed in human cancers, indicating that small RNAs may have a part to play in tumour suppression. However, little is known about how miRNA expression is regulated. Gregory J. Hannon and colleagues compared the miRNA expression profiles of wild-type and p53-deficient mouse cells. They identified a family of non-coding miRNAs — miR-34 — that is the direct target of, and thus regulated by, p53, and show that the ectopic expression of these miRNAs leads to growth arrest and, in some cases, cell senescence. This suggests that the miR-34 family acts as components of p53-mediated growth and arrest pathways, and the authors describe several miR-34 target genes that have roles in cell cycle progression.
miR-34 is one of only 18 mammalian miRNA families that are also present in Drosophila and the nematode worm Caenorhabditis elegans. This raises the possibility that the link between p53 and miR-34 might have arisen early in the evolution of the p53 network and may be important in p53 function in diverse species, the authors speculate. The paper represents one of the first discoveries of direct transcriptional regulators for miRNAs and is likely to be the tip of the iceberg.
CONTACT
Gregory J. Hannon (Cold Spring Harbor Laboratory, NY, USA)
Tel: +1 516 367 8889; E-mail: hannon@cshl.org
The tumour suppressor p53 acts directly on a family of small RNAs that are vital for cell growth and replication. Already well known for its indirect effects, p53 is now shown to target the miR-34 family of microRNAs (miRNAs), which itself suppresses cell proliferation.
A global decrease in miRNA levels is often observed in human cancers, indicating that small RNAs may have a part to play in tumour suppression. However, little is known about how miRNA expression is regulated. Gregory J. Hannon and colleagues compared the miRNA expression profiles of wild-type and p53-deficient mouse cells. They identified a family of non-coding miRNAs — miR-34 — that is the direct target of, and thus regulated by, p53, and show that the ectopic expression of these miRNAs leads to growth arrest and, in some cases, cell senescence. This suggests that the miR-34 family acts as components of p53-mediated growth and arrest pathways, and the authors describe several miR-34 target genes that have roles in cell cycle progression.
miR-34 is one of only 18 mammalian miRNA families that are also present in Drosophila and the nematode worm Caenorhabditis elegans. This raises the possibility that the link between p53 and miR-34 might have arisen early in the evolution of the p53 network and may be important in p53 function in diverse species, the authors speculate. The paper represents one of the first discoveries of direct transcriptional regulators for miRNAs and is likely to be the tip of the iceberg.
CONTACT
Gregory J. Hannon (Cold Spring Harbor Laboratory, NY, USA)
Tel: +1 516 367 8889; E-mail: hannon@cshl.org
Stem cells: DNA damage contributes to stem cell ageing
DNA damage can cause premature ageing in bone-marrow-derived stem cells, making it harder for them to function. The finding has implications for the use of adult stem cells in transplantation.
Long-lived multicellular organisms depend on small pools of slowly dividing stem cells to replenish lost tissue, and it's important that these reserves are self-renewed and maintained with minimal mutations throughout life.
Derrick J. Rossi and colleagues now show that blood-forming stem cells from the bone marrow of mice accumulate DNA damage with age. This, they say, might underlie the reduced capacity of stem cells to yield new tissues and repair injury over time.
Richard J. Cornall and colleagues studied bone-marrow-derived stem cells from a mouse strain that has problems repairing DNA damage, and arrived at a similar conclusion — under physiological conditions, unrepaired DNA damage in stem cells can lead to an age-dependent decline in their numbers.
CONTACT
Derrick J. Rossi (Stanford University, CA, USA) Author paper [5]
Tel: +1 650 723 7389; E-mail: drossi@stanford.edu
Richard J. Cornall (Oxford University, UK) Author paper [6]
Tel: +44 1865 287 790; E-mail: richard.cornall@ndm.ox.ac.uk
DNA damage can cause premature ageing in bone-marrow-derived stem cells, making it harder for them to function. The finding has implications for the use of adult stem cells in transplantation.
Long-lived multicellular organisms depend on small pools of slowly dividing stem cells to replenish lost tissue, and it's important that these reserves are self-renewed and maintained with minimal mutations throughout life.
Derrick J. Rossi and colleagues now show that blood-forming stem cells from the bone marrow of mice accumulate DNA damage with age. This, they say, might underlie the reduced capacity of stem cells to yield new tissues and repair injury over time.
Richard J. Cornall and colleagues studied bone-marrow-derived stem cells from a mouse strain that has problems repairing DNA damage, and arrived at a similar conclusion — under physiological conditions, unrepaired DNA damage in stem cells can lead to an age-dependent decline in their numbers.
CONTACT
Derrick J. Rossi (Stanford University, CA, USA) Author paper [5]
Tel: +1 650 723 7389; E-mail: drossi@stanford.edu
Richard J. Cornall (Oxford University, UK) Author paper [6]
Tel: +44 1865 287 790; E-mail: richard.cornall@ndm.ox.ac.uk
Metabolic disease: Potential drug for atherosclerosis and type 2 diseases
A small-molecule inhibitor that has been successfully tested in mice may prove useful against chronic metabolic diseases such as atherosclerosis, obesity and type 2 diabetes.
Gökhan S. Hotamisligil and colleagues treated genetic mice models of various metabolic diseases with a drug that inhibits a protein called aP2. When given orally, the drug molecule reduced the size of atherosclerotic lesions in blood vessels. It also decreased blood glucose levels and increased insulin sensitivity in a model of obesity and insulin resistance.
aP2 is expressed in fat cells and scavenging white blood cells called macrophages, where it mediates metabolic and inflammatory reactions. It's already known that mice genetically manipulated to lack the protein are protected against various aspects of metabolic disease, suggesting that aP2 may prove a useful drug target for these conditions. This study backs this idea up, hinting that aP2 inhibitors may aid the treatment of human cardiovascular disease and diabetes.
CONTACT
Gökhan S. Hotamisligil (Harvard School of Public Health, Boston, MA, USA)
Tel: +1 617 432 1950; E-mail: ghotamis@hsph.harvard.edu
A small-molecule inhibitor that has been successfully tested in mice may prove useful against chronic metabolic diseases such as atherosclerosis, obesity and type 2 diabetes.
Gökhan S. Hotamisligil and colleagues treated genetic mice models of various metabolic diseases with a drug that inhibits a protein called aP2. When given orally, the drug molecule reduced the size of atherosclerotic lesions in blood vessels. It also decreased blood glucose levels and increased insulin sensitivity in a model of obesity and insulin resistance.
aP2 is expressed in fat cells and scavenging white blood cells called macrophages, where it mediates metabolic and inflammatory reactions. It's already known that mice genetically manipulated to lack the protein are protected against various aspects of metabolic disease, suggesting that aP2 may prove a useful drug target for these conditions. This study backs this idea up, hinting that aP2 inhibitors may aid the treatment of human cardiovascular disease and diabetes.
CONTACT
Gökhan S. Hotamisligil (Harvard School of Public Health, Boston, MA, USA)
Tel: +1 617 432 1950; E-mail: ghotamis@hsph.harvard.edu
Genomics: Insights into seven diseases revealed
The true potential of the human genome is uncovered. The study compares 2,000 cases each of seven common diseases with 3,000 shared control patients, and unveils new genetic associations with these disorders. A pair of related papers in Nature Genetics offer further insights into two of the seven diseases investigated.
In the Nature article, researchers from the Wellcome Trust Case Control Consortium report genetic variants associated with the development of bipolar disorder, Crohn’s disease, coronary heart disease, type 1 and type 2 diabetes, rheumatoid arthritis and hypertension. In the first study from this large scope, the scientists found one genetic region newly associated with bipolar disorder, and another with coronary artery disease. A separate group of three markers are associated with rheumatoid arthritis. The authors also identify nine new genetic associations for Crohn’s disease and ten chromosome regions that contain genes related to diabetes.
Separate papers in Nature Genetics support the new insights into the chromosome regions involved in Crohn’s disease—reporting strong association for six new loci—and detail replication of some of the results for type 1 diabetes.
Peter Donnelly, Miles Parkes, John Todd and colleagues believe their findings offer avenues of research for each of the seven disorders. This work represents a major step towards dissecting the biological bases of common diseases; future work is already focusing on translating the findings into improvements in human health.
CONTACT
Peter Donnelly (Chair, Wellcome Trust Case Control Consortium, University of Oxford, UK)
Author paper [1]
Tel: +44 1865 285 385; E-mail: donnelly@stats.ox.ac.uk
Craig Brierley (Media Officer, Wellcome Trust, London, UK)
Tel: +44 20 7611 7329; E-mail: c.brierley@wellcome.ac.uk
Anne M. Bowcock (Washington University School of Medicine, St Louis, MO, USA) N&V author
Tel: +1 314 747 3264; E-mail: bowcock@genetics.wustl.edu
The true potential of the human genome is uncovered. The study compares 2,000 cases each of seven common diseases with 3,000 shared control patients, and unveils new genetic associations with these disorders. A pair of related papers in Nature Genetics offer further insights into two of the seven diseases investigated.
In the Nature article, researchers from the Wellcome Trust Case Control Consortium report genetic variants associated with the development of bipolar disorder, Crohn’s disease, coronary heart disease, type 1 and type 2 diabetes, rheumatoid arthritis and hypertension. In the first study from this large scope, the scientists found one genetic region newly associated with bipolar disorder, and another with coronary artery disease. A separate group of three markers are associated with rheumatoid arthritis. The authors also identify nine new genetic associations for Crohn’s disease and ten chromosome regions that contain genes related to diabetes.
Separate papers in Nature Genetics support the new insights into the chromosome regions involved in Crohn’s disease—reporting strong association for six new loci—and detail replication of some of the results for type 1 diabetes.
Peter Donnelly, Miles Parkes, John Todd and colleagues believe their findings offer avenues of research for each of the seven disorders. This work represents a major step towards dissecting the biological bases of common diseases; future work is already focusing on translating the findings into improvements in human health.
CONTACT
Peter Donnelly (Chair, Wellcome Trust Case Control Consortium, University of Oxford, UK)
Author paper [1]
Tel: +44 1865 285 385; E-mail: donnelly@stats.ox.ac.uk
Craig Brierley (Media Officer, Wellcome Trust, London, UK)
Tel: +44 20 7611 7329; E-mail: c.brierley@wellcome.ac.uk
Anne M. Bowcock (Washington University School of Medicine, St Louis, MO, USA) N&V author
Tel: +1 314 747 3264; E-mail: bowcock@genetics.wustl.edu
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