New genetic risk factor for type 2 diabetes
Variation in the gene called CDKAL1 is associated with risk of developing type 2 diabetes.
Valgerdur Steinthorsdottir and colleagues discovered this new risk variant through a large-scale survey in Iceland in which they compared the frequencies of several hundred thousand common genetic variants in healthy individuals with those who have the disease. They subsequently replicated the association between type 2 diabetes and a variant in CDKAL1 in samples from several independent populations of European or Han Chinese ancestry. Individuals with two copies of the risk variant were found to be at increased risk for developing disease compared to individuals with only a single copy of the risk variant. Such individuals also had approximately 20% less insulin response than individuals with only one copy or non-carriers, suggesting that the variant may confer risk of type 2 diabetes through reduced insulin secretion.
Author contacts:
Edward Farmer (Director of Corporate Communication, deCODE genetics Inc)
Tel: +1 646 417 4555; E-mail: edward.farmer@decode.is
Valgerdur Steinthorsdottir (deCODE Genetics, Reykjavik, Iceland)
E-mail: vstein@decode.is
Kari Stefansson (deCODE Genetics, Reykjavik, Iceland)
E-mail: kstefans@decode.is
Sunday, April 29, 2007
Sunday, April 22, 2007
Increasing bad cholesterol levels
A study of Nature Structural & Molecular Biology suggests how the gene PCSK9 maintains cholesterol balance in the body.
Low-density lipoproteins (LDLs, also known as ‘bad cholesterol’) are removed from the bloodstream by binding to LDL receptors (LDLRs) present on the surface of cells. After binding, cells internalize both the receptor and cholesterol, the cholesterol is processed by the cell and LDLR is recycled back to the surface, where it can bind new cholesterol molecules. The amount of surface LDLR is decreased by the PCSK9 protein, resulting in high blood cholesterol, but how PCSK9 does this was not known.
Xiayang Qiu and colleagues have now found that PCSK9 binds very tightly to LDLR. This tight binding may lower LDLR levels on the cell surface by sequestering LDLRs inside cells, preventing their recycling back to the cell surface. A mutation in PCSK9 associated with high cholesterol shows even tighter binding to LDLR, supporting this model. These findings should improve our understanding of cholesterol regulation, and may help in the development of drugs to treat cardiovascular disease.
Author contact:
Xiayang Qiu (Pfizer, Groton, CT, USA)
Tel: +1 860 715 6718; E-mail: xiayang.qiu@pfizer.com
A study of Nature Structural & Molecular Biology suggests how the gene PCSK9 maintains cholesterol balance in the body.
Low-density lipoproteins (LDLs, also known as ‘bad cholesterol’) are removed from the bloodstream by binding to LDL receptors (LDLRs) present on the surface of cells. After binding, cells internalize both the receptor and cholesterol, the cholesterol is processed by the cell and LDLR is recycled back to the surface, where it can bind new cholesterol molecules. The amount of surface LDLR is decreased by the PCSK9 protein, resulting in high blood cholesterol, but how PCSK9 does this was not known.
Xiayang Qiu and colleagues have now found that PCSK9 binds very tightly to LDLR. This tight binding may lower LDLR levels on the cell surface by sequestering LDLRs inside cells, preventing their recycling back to the cell surface. A mutation in PCSK9 associated with high cholesterol shows even tighter binding to LDLR, supporting this model. These findings should improve our understanding of cholesterol regulation, and may help in the development of drugs to treat cardiovascular disease.
Author contact:
Xiayang Qiu (Pfizer, Groton, CT, USA)
Tel: +1 860 715 6718; E-mail: xiayang.qiu@pfizer.com
Astrocytes kill neurons in ALS
Astrocytes carrying a mutated version of a protein that causes amyotrophic lateral sclerosis (ALS, also known as Lou Gehrig’s disease) are responsible for the death of motor neurons, report two papers in the May issue of Nature Neuroscience. These findings suggest that stem cell therapy focused on replacing damaged neurons may not be feasible in ALS, because diseased astrocytes would be expected to damage the replacement neurons.
Mutations in the gene for superoxide dismutase (SOD1) cause some cases of ALS, in which progressive degeneration of motor neurons leads to paralysis and eventually death. In both studies, the authors expressed this mutant protein in single cell types in culture. Motor neurons degenerated and died when cocultured with astrocytes expressing mutant SOD1, while mutant SOD1 in neurons, fibroblasts or microglia did not cause neuronal death.
Przedborski and colleagues additionally report that the astrocytes expressing mutant SOD1 killed only the neurons that degenerate in ALS, not other types of neurons, and that this was due to a soluble toxic factor released by the astrocytes. If this toxic factor can be identified in future studies, this finding may offer novel strategies for therapy.
Author contacts:
Serge Przedborski (Columbia University, New York, NY, USA) Paper [7]
Tel: +1 212 305 1540; E-mail: sp30@columbia.edu
Kevin Eggan (Harvard University, Cambridge, MA, USA) Paper [8]
Tel: +1 617 496 5611; E-mail: eggan@mcb.harvard.edu
Additional contact for comment on papers:
Jean-Pierre Julien (Laval University, Québec, Canada)
Tel: +1 418 654 2296; E-mail: jean-pierre.julien@crchul.ulaval.ca
Astrocytes carrying a mutated version of a protein that causes amyotrophic lateral sclerosis (ALS, also known as Lou Gehrig’s disease) are responsible for the death of motor neurons, report two papers in the May issue of Nature Neuroscience. These findings suggest that stem cell therapy focused on replacing damaged neurons may not be feasible in ALS, because diseased astrocytes would be expected to damage the replacement neurons.
Mutations in the gene for superoxide dismutase (SOD1) cause some cases of ALS, in which progressive degeneration of motor neurons leads to paralysis and eventually death. In both studies, the authors expressed this mutant protein in single cell types in culture. Motor neurons degenerated and died when cocultured with astrocytes expressing mutant SOD1, while mutant SOD1 in neurons, fibroblasts or microglia did not cause neuronal death.
Przedborski and colleagues additionally report that the astrocytes expressing mutant SOD1 killed only the neurons that degenerate in ALS, not other types of neurons, and that this was due to a soluble toxic factor released by the astrocytes. If this toxic factor can be identified in future studies, this finding may offer novel strategies for therapy.
Author contacts:
Serge Przedborski (Columbia University, New York, NY, USA) Paper [7]
Tel: +1 212 305 1540; E-mail: sp30@columbia.edu
Kevin Eggan (Harvard University, Cambridge, MA, USA) Paper [8]
Tel: +1 617 496 5611; E-mail: eggan@mcb.harvard.edu
Additional contact for comment on papers:
Jean-Pierre Julien (Laval University, Québec, Canada)
Tel: +1 418 654 2296; E-mail: jean-pierre.julien@crchul.ulaval.ca
Mutation leads to male infertility
A mutation in a gene called AURKC (Aurora Kinase C) has been identified in 14 infertile men of North African descent. While deletions of some portion of the Y chromosome have been found in infertile men, this is a rare example in which a mutation in a single gene causes male infertility.
Estimates suggest that at least 80 million individuals worldwide are infertile. Pierre Ray and colleagues studied 14 men whose infertility seemed to have a similar origin. Their sperm were characterized by large heads, increased DNA content, and a variable number of flagella—the whip-like tails that propel the sperm. A genome-wide scan identified a mutation in AURKC that severely truncates the protein. AURKC encodes an enzyme that phosphorylates other proteins, and the authors show that the mutation abolishes this activity. An analysis of the genomic region around AURKC shows that these individuals have other markers in common, suggesting that this mutation appeared in a North African common ancestor approximately 1,500 years ago. The authors note that a larger study of the prevalence of this mutation in North Africans is now warranted.
Author contact:
Pierre Ray (University Hospital of Grenoble, France)
Tel: +33 476 76 55 73; E-mail: pray@chu-grenoble.fr
A mutation in a gene called AURKC (Aurora Kinase C) has been identified in 14 infertile men of North African descent. While deletions of some portion of the Y chromosome have been found in infertile men, this is a rare example in which a mutation in a single gene causes male infertility.
Estimates suggest that at least 80 million individuals worldwide are infertile. Pierre Ray and colleagues studied 14 men whose infertility seemed to have a similar origin. Their sperm were characterized by large heads, increased DNA content, and a variable number of flagella—the whip-like tails that propel the sperm. A genome-wide scan identified a mutation in AURKC that severely truncates the protein. AURKC encodes an enzyme that phosphorylates other proteins, and the authors show that the mutation abolishes this activity. An analysis of the genomic region around AURKC shows that these individuals have other markers in common, suggesting that this mutation appeared in a North African common ancestor approximately 1,500 years ago. The authors note that a larger study of the prevalence of this mutation in North Africans is now warranted.
Author contact:
Pierre Ray (University Hospital of Grenoble, France)
Tel: +33 476 76 55 73; E-mail: pray@chu-grenoble.fr
Genetic susceptibility to Crohn disease
A genome-wide assessment of genetic variation in individuals with Crohn disease has identified seven genes or regions that are associated with elevated risk of the disease, according to a study.Three of the genes were previously known, but four are newly associated with the disease.
Crohn disease is one of the most common forms of inflammatory bowel disease, affecting 100–150 per 100,000 individuals of European ancestry. John Rioux and colleagues assessed more than 300,000 genetic variants in individuals with Crohn disease, as well as controls, and identified three previously reported risk factors (CARD15, IL23R, and ATG16L1), and four new ones (PHOX2B, NCF4, FAM92B, and a region on chromosome 10).
In combination with other studies, these ‘genome-wide association studies’ promise to flesh out the entire catalogue of genetic variants that predispose to Crohn disease, as well as provide new insight into the causes of the disease. In this case, the authors show that ATG16L1 might have a role in the degradation and processing of bacteria by the body’s inflammatory response—a process known as autophagy. This is consistent with other evidence that an inappropriate response to bacteria in the gut is important in the initiation of Crohn disease.
Author contact:
John Rioux (University of Montreal, Québec, Canada)
Tel: +1 514 376 3330; E-mail: rioux@broad.mit.edu
A genome-wide assessment of genetic variation in individuals with Crohn disease has identified seven genes or regions that are associated with elevated risk of the disease, according to a study.Three of the genes were previously known, but four are newly associated with the disease.
Crohn disease is one of the most common forms of inflammatory bowel disease, affecting 100–150 per 100,000 individuals of European ancestry. John Rioux and colleagues assessed more than 300,000 genetic variants in individuals with Crohn disease, as well as controls, and identified three previously reported risk factors (CARD15, IL23R, and ATG16L1), and four new ones (PHOX2B, NCF4, FAM92B, and a region on chromosome 10).
In combination with other studies, these ‘genome-wide association studies’ promise to flesh out the entire catalogue of genetic variants that predispose to Crohn disease, as well as provide new insight into the causes of the disease. In this case, the authors show that ATG16L1 might have a role in the degradation and processing of bacteria by the body’s inflammatory response—a process known as autophagy. This is consistent with other evidence that an inappropriate response to bacteria in the gut is important in the initiation of Crohn disease.
Author contact:
John Rioux (University of Montreal, Québec, Canada)
Tel: +1 514 376 3330; E-mail: rioux@broad.mit.edu
Friday, April 20, 2007
IMPORTANT ANNOUNCEMENT AND INFORMATIONS
EAGLES Health Lecturer Tour Grants
The European Action on Global Life Sciences (EAGLES) Health Programme is offering grants of up to €5,000 to leading biomedical scientists and other health specialists, including commentators and journalists, from developing countries to undertake lecture tours around Europe to communicate the needs of developing countries to the European public and European institutions. Applications should be submitted before 11 June 2007. Further details can be found on the EAGLES website: www.efb-central.org/eagles/site.
International Workshop on Cities, Science and Sustainability
An international workshop examining successful approaches to 'cities, science and sustainability' will be held at TWAS's headquarters in Trieste, Italy, from 20 to 22 September 2007. Institutions in developing countries are invited to respond by 1 July 2007 indicating their interest in participating in the workshop and presenting a report highlighting successful initiatives in using science and technology in solving problems of sustainability associated with large urban areas, including (but not limited to) access to safe drinking water, sanitation, air pollution, housing and construction, land use planning, transport, traffic congestion and waste disposal in a city in the developing world. The project 'Cities, Science and Sustainability' is a collaborative effort between TWAS, the Consortium for Science, Technology and Innovation for the South (COSTIS) and the United Nations Development Programme's Special Unit for South-South Cooperation (UNDP-SSC).
African Materials Research Conference in December
The 4th International Conference of the African Materials Research Society will be held in Dar-es-Salaam, Tanzania, from 10 to 14 December 2007. Main topic of the conference: "Cementing Collaborations in Materials Research in Africa." Deadline for pre-registration and abstracts: 30 June 2007
Award in Medical Sciences in the UAE
The 'Sheikh Hamdan Bin Rashid Al Maktoum Awards for Medical Sciences' (SHAMS) are accepting nominations in three categories: international, Arab world, and UAE. The awards honour "medical researchers worldwide who enrich scientific research and enhance the nature of scientific exchanges among medical doctors in UAE and medical centers abroad." Deadline for nominations is November. For more information on the Awards, please visit: www.hmaward.org.ae
EAGLES Health Lecturer Tour Grants
The European Action on Global Life Sciences (EAGLES) Health Programme is offering grants of up to €5,000 to leading biomedical scientists and other health specialists, including commentators and journalists, from developing countries to undertake lecture tours around Europe to communicate the needs of developing countries to the European public and European institutions. Applications should be submitted before 11 June 2007. Further details can be found on the EAGLES website: www.efb-central.org/eagles/site.
International Workshop on Cities, Science and Sustainability
An international workshop examining successful approaches to 'cities, science and sustainability' will be held at TWAS's headquarters in Trieste, Italy, from 20 to 22 September 2007. Institutions in developing countries are invited to respond by 1 July 2007 indicating their interest in participating in the workshop and presenting a report highlighting successful initiatives in using science and technology in solving problems of sustainability associated with large urban areas, including (but not limited to) access to safe drinking water, sanitation, air pollution, housing and construction, land use planning, transport, traffic congestion and waste disposal in a city in the developing world. The project 'Cities, Science and Sustainability' is a collaborative effort between TWAS, the Consortium for Science, Technology and Innovation for the South (COSTIS) and the United Nations Development Programme's Special Unit for South-South Cooperation (UNDP-SSC).
African Materials Research Conference in December
The 4th International Conference of the African Materials Research Society will be held in Dar-es-Salaam, Tanzania, from 10 to 14 December 2007. Main topic of the conference: "Cementing Collaborations in Materials Research in Africa." Deadline for pre-registration and abstracts: 30 June 2007
Award in Medical Sciences in the UAE
The 'Sheikh Hamdan Bin Rashid Al Maktoum Awards for Medical Sciences' (SHAMS) are accepting nominations in three categories: international, Arab world, and UAE. The awards honour "medical researchers worldwide who enrich scientific research and enhance the nature of scientific exchanges among medical doctors in UAE and medical centers abroad." Deadline for nominations is November. For more information on the Awards, please visit: www.hmaward.org.ae
Fossils: Tell it to the trees
A spectacular fossilized tree gives an unprecedented insight into the appearance of the world’s earliest forests.
William E. Stein and colleagues found their fossil tree in Schoharie County, New York. It stood at least eight metres high with fern-like branches, a long trunk and small anchoring roots. Its crown belongs to a previously known plant taxon, the cladoxylopsid Wattieza. But its trunk and base match a different group, named Eospermatopteris.
The evolution of trees was fundamental to the Earth’s terrestrial ecosystem. And until now, the earliest-known evidence of forests came from fossil tree stumps found in Gilboa, New York, that are about 385 million years old. The trees were designated Eospermatopteris but their aerial portions were missing. The new find sheds light on their possible full appearance.
CONTACT
William E. Stein (State University of New York, Binghamton, NY, USA)
Tel: +1 607 777 4391; E-mail: stein@binghamton.edu
Albert Gnidica (Media Relations, New York State Museum, NY, USA)
Tel: +1 518 474 0068 or +1 518 474 8730; E-mail: Agnidica@mail.nysed.gov
Brigitte Meyer-Berthaud (CIRAD-CNRS, Montpellier, France) N&V author
Tel: +33 4 67 61 75 22; E-mail: meyerberthaud@cirad.fr
A spectacular fossilized tree gives an unprecedented insight into the appearance of the world’s earliest forests.
William E. Stein and colleagues found their fossil tree in Schoharie County, New York. It stood at least eight metres high with fern-like branches, a long trunk and small anchoring roots. Its crown belongs to a previously known plant taxon, the cladoxylopsid Wattieza. But its trunk and base match a different group, named Eospermatopteris.
The evolution of trees was fundamental to the Earth’s terrestrial ecosystem. And until now, the earliest-known evidence of forests came from fossil tree stumps found in Gilboa, New York, that are about 385 million years old. The trees were designated Eospermatopteris but their aerial portions were missing. The new find sheds light on their possible full appearance.
CONTACT
William E. Stein (State University of New York, Binghamton, NY, USA)
Tel: +1 607 777 4391; E-mail: stein@binghamton.edu
Albert Gnidica (Media Relations, New York State Museum, NY, USA)
Tel: +1 518 474 0068 or +1 518 474 8730; E-mail: Agnidica@mail.nysed.gov
Brigitte Meyer-Berthaud (CIRAD-CNRS, Montpellier, France) N&V author
Tel: +33 4 67 61 75 22; E-mail: meyerberthaud@cirad.fr
Geology: The big melts
The Earth’s continental crust was not formed gradually but in stages, punctuated by large, potentially global, melting events. A report analyses the helium isotopic ratios from ocean island basalts, which reveal several distinct episodes of crustal growth.
Most Earth scientists agree that the continental crust formed by a process of partial melting from the mantle, although the timing and details of this process has remained controversial. Stephen Parman studied the chemical fingerprint of continental crust formation in the isotopic composition of helium isotopes recorded in ocean island basalts. The volatility of helium isotopes means that they are not reintroduced into the mantle during subduction and the record of mantle depletion is thus preserved for helium, whereas most other isotopes are continually recycled by mantle convection, largely obscuring such a record.
Parman found that peaks in the occurrence of helium isotope ratios are globally consistent and correspond with the ages of what have been proposed to be continental growth pulses. He concludes that the ultimate cause of these large melting events is still unclear, but could be related to large releases of heat from the mantle.
CONTACT
Stephen Parman (University of Durham, UK)
E-mail: stephen.parman@durham.ac.uk
Please note that the author is travelling in the US but should be contactable by email and mobile: Tel: +1 302 588 7369
Don Porcelli (University of Oxford, UK) N&V author
Tel: +44 1865 282 121; E-mail: don.porcelli@earth.ox.ac.uk
The Earth’s continental crust was not formed gradually but in stages, punctuated by large, potentially global, melting events. A report analyses the helium isotopic ratios from ocean island basalts, which reveal several distinct episodes of crustal growth.
Most Earth scientists agree that the continental crust formed by a process of partial melting from the mantle, although the timing and details of this process has remained controversial. Stephen Parman studied the chemical fingerprint of continental crust formation in the isotopic composition of helium isotopes recorded in ocean island basalts. The volatility of helium isotopes means that they are not reintroduced into the mantle during subduction and the record of mantle depletion is thus preserved for helium, whereas most other isotopes are continually recycled by mantle convection, largely obscuring such a record.
Parman found that peaks in the occurrence of helium isotope ratios are globally consistent and correspond with the ages of what have been proposed to be continental growth pulses. He concludes that the ultimate cause of these large melting events is still unclear, but could be related to large releases of heat from the mantle.
CONTACT
Stephen Parman (University of Durham, UK)
E-mail: stephen.parman@durham.ac.uk
Please note that the author is travelling in the US but should be contactable by email and mobile: Tel: +1 302 588 7369
Don Porcelli (University of Oxford, UK) N&V author
Tel: +44 1865 282 121; E-mail: don.porcelli@earth.ox.ac.uk
Quantum physics: Losing a grip on realit
It seems common sense that an object will retain its fundamental properties regardless of whether or not we are looking at it. But in the microscopic quantum world, everyday rules do not apply. Even our concept of reality may be challenged.
Classical physics clings tightly to the notions of realism (where external reality exists independent of observation) and locality (where sufficiently distant objects cannot influence each other). Quantum experiments in which the properties of distant but entangled particles are linked seem hard to reconcile with such notions, making local realistic theories untenable.
Markus Aspelmeyer, Anton Zeilinger and colleagues developed an inequality that relaxes the assumption of locality, allowing a test of non-local realism. They studied correlations between pairs of entangled photons, and found that the correlations violate non-local realistic theories. The result suggests that giving up the concept of locality is not sufficient to be consistent with quantum experiments, unless certain intuitive features of realism are abandoned.
CONTACT
Markus Aspelmeyer (University of Vienna, Austria)
Please contact the author through:
Ursula Gerber (University of Vienna, Austria)
Tel: +43 1 4277 51205; E-mail: ursula.gerber@univie.ac.at
Alain Aspect (Institut d'Optique, Palaiseau, France) N&V author
Tel: +33 1 64 53 31 03; E-mail: alain.aspect@institutoptique.fr
It seems common sense that an object will retain its fundamental properties regardless of whether or not we are looking at it. But in the microscopic quantum world, everyday rules do not apply. Even our concept of reality may be challenged.
Classical physics clings tightly to the notions of realism (where external reality exists independent of observation) and locality (where sufficiently distant objects cannot influence each other). Quantum experiments in which the properties of distant but entangled particles are linked seem hard to reconcile with such notions, making local realistic theories untenable.
Markus Aspelmeyer, Anton Zeilinger and colleagues developed an inequality that relaxes the assumption of locality, allowing a test of non-local realism. They studied correlations between pairs of entangled photons, and found that the correlations violate non-local realistic theories. The result suggests that giving up the concept of locality is not sufficient to be consistent with quantum experiments, unless certain intuitive features of realism are abandoned.
CONTACT
Markus Aspelmeyer (University of Vienna, Austria)
Please contact the author through:
Ursula Gerber (University of Vienna, Austria)
Tel: +43 1 4277 51205; E-mail: ursula.gerber@univie.ac.at
Alain Aspect (Institut d'Optique, Palaiseau, France) N&V author
Tel: +33 1 64 53 31 03; E-mail: alain.aspect@institutoptique.fr
Announcement-Four leading researchers from Japan and the UK meet in London to present:
“Frontiers of Neuroscience” Major advancements in medical research and their applications
Keio University, University College London (UCL), and Japan Society for the Promotion of Science (JSPS), London Office will host the Keio University 150th Anniversary International Symposium, “Frontiers of Neuroscience”. Four leading scholars specialising in neuroscience will present their cutting-edge research and discuss its potential for curing today’s most devastating injuries and diseases of the brain. The event, which is free and open to the public, will take place on April 27 from 3 p.m. to 6 p.m. at UCL’s Cruciform Lecture Theatre 2, Gower Street, London, UK.
Two island countries, two universities, four scientists and an office
Two universities, on two island countries at either end of the Eurasian continent, have played a leading role in the liberalisation of science and education from their respective beginnings, in 1826 (UCL) and 1858 (Keio), that continues today. Four pioneering scientists, two from each university, will gather on the UCL campus for an international symposium exploring issues surrounding ground-breaking advancements in neuroscience and related topics relevant to our current, fast-changing society. In addition to promoting collaboration between the three participating organizations and celebrating the 150th anniversary of Keio University, the event will commemorate the launch of the Keio University London Office, established in alliance with JSPS.
Frontiers of Neuroscience – Opportunities for better understanding ourselves –
Keio University’s Prof Hideyuki Okano is a specialist in damaged Central Nervous System (CNS) regeneration. His current research is breaking new ground in adult neurogenesis (birth of new neuronal cells) and brain damage repair, and may open up a number of possibilities including therapeutic intervention for spinal cord injuries and treatments for neurodegenerative disorders including Alzheimer's disease. He will discuss both the principles of regeneration and his research group’s latest findings. Prof Masato Yasui, also from Keio University, specialises in a class of integral membrane proteins known as aquaporin, which functions as a channel for transporting water through biological cell membranes. Aquaporin is a recent discovery, and has led to a series of studies into its relation to a wide range of human diseases. Prof Yasui’s interest is in aquaporin-4 (AQP4), a particular type of aquaporin that is predominantly expressed in mammalian brains. On the basis of precedent findings, including its involvement in brain edema formation, he will discuss potential connections between AQP4 and mental disorders such as bipolar diseases.
Participating scientists from UCL are prominent authorities on the fundamentals of brain function. Prof Richard Frackowiak, a specialist in brain plasticity and recovery from injury, is conducting pioneering research that is serving to clarify the relationship between the brain’s functions and its physical structure. His lecture will focus on brain organisation as observed using advanced imaging technologies and methods. Prof Semir Zeki’s research focuses on the relationship between vision, art and the brain. He has lectured on the subject worldwide and is the founder of the Institute of Neuroesthetics. His insightful and careful analyses suggest that visual consciousness is distributed in both time and space. Prof Zeki will discuss the nature of visual consciousnesses in his lecture.
The symposium will begin with a welcome from Prof Yuichiro Anzai, president of Keio University and an eminent cognitive scientist, followed by the four lectures and a panel discussion. It will conclude with a reception at 6 p.m.
Members of the press are invited to attend the symposium, which is free and open to the public. Interview requests can be forwarded to press contact Juli Morizawa (Ms) or Akiko Kurata (Ms).
For more information and to register, visit http://keio150.jp/english/events/2007/20070427e.html or email sympo-rsvp@adst.keio.ac.jp.
General Inquiries: Yuko Sakuma (Ms)
International Programme Coordinator, Keio University London Office, UK
Email: sympo-rsvp@adst.keio.ac.jp Tel: (020) 7629 3577 Fax: (020) 7629 3588
Media Inquiries: Juli Morizawa (Ms), Akiko Kurata (Ms)
Office of Communications and Public Relations, Keio University, Japan
Email: m-koho@adst.keio.ac.jp Tel: +81-3-5427-1541 Fax: +81-3-5441-7640
Meeting information
“Frontiers of Neuroscience” April 27 (3 p.m. to 6 p.m.) at UCL’s Cruciform Lecture Theatre 2, Gower Street, London, UK.
“Frontiers of Neuroscience” Major advancements in medical research and their applications
Keio University, University College London (UCL), and Japan Society for the Promotion of Science (JSPS), London Office will host the Keio University 150th Anniversary International Symposium, “Frontiers of Neuroscience”. Four leading scholars specialising in neuroscience will present their cutting-edge research and discuss its potential for curing today’s most devastating injuries and diseases of the brain. The event, which is free and open to the public, will take place on April 27 from 3 p.m. to 6 p.m. at UCL’s Cruciform Lecture Theatre 2, Gower Street, London, UK.
Two island countries, two universities, four scientists and an office
Two universities, on two island countries at either end of the Eurasian continent, have played a leading role in the liberalisation of science and education from their respective beginnings, in 1826 (UCL) and 1858 (Keio), that continues today. Four pioneering scientists, two from each university, will gather on the UCL campus for an international symposium exploring issues surrounding ground-breaking advancements in neuroscience and related topics relevant to our current, fast-changing society. In addition to promoting collaboration between the three participating organizations and celebrating the 150th anniversary of Keio University, the event will commemorate the launch of the Keio University London Office, established in alliance with JSPS.
Frontiers of Neuroscience – Opportunities for better understanding ourselves –
Keio University’s Prof Hideyuki Okano is a specialist in damaged Central Nervous System (CNS) regeneration. His current research is breaking new ground in adult neurogenesis (birth of new neuronal cells) and brain damage repair, and may open up a number of possibilities including therapeutic intervention for spinal cord injuries and treatments for neurodegenerative disorders including Alzheimer's disease. He will discuss both the principles of regeneration and his research group’s latest findings. Prof Masato Yasui, also from Keio University, specialises in a class of integral membrane proteins known as aquaporin, which functions as a channel for transporting water through biological cell membranes. Aquaporin is a recent discovery, and has led to a series of studies into its relation to a wide range of human diseases. Prof Yasui’s interest is in aquaporin-4 (AQP4), a particular type of aquaporin that is predominantly expressed in mammalian brains. On the basis of precedent findings, including its involvement in brain edema formation, he will discuss potential connections between AQP4 and mental disorders such as bipolar diseases.
Participating scientists from UCL are prominent authorities on the fundamentals of brain function. Prof Richard Frackowiak, a specialist in brain plasticity and recovery from injury, is conducting pioneering research that is serving to clarify the relationship between the brain’s functions and its physical structure. His lecture will focus on brain organisation as observed using advanced imaging technologies and methods. Prof Semir Zeki’s research focuses on the relationship between vision, art and the brain. He has lectured on the subject worldwide and is the founder of the Institute of Neuroesthetics. His insightful and careful analyses suggest that visual consciousness is distributed in both time and space. Prof Zeki will discuss the nature of visual consciousnesses in his lecture.
The symposium will begin with a welcome from Prof Yuichiro Anzai, president of Keio University and an eminent cognitive scientist, followed by the four lectures and a panel discussion. It will conclude with a reception at 6 p.m.
Members of the press are invited to attend the symposium, which is free and open to the public. Interview requests can be forwarded to press contact Juli Morizawa (Ms) or Akiko Kurata (Ms).
For more information and to register, visit http://keio150.jp/english/events/2007/20070427e.html or email sympo-rsvp@adst.keio.ac.jp.
General Inquiries: Yuko Sakuma (Ms)
International Programme Coordinator, Keio University London Office, UK
Email: sympo-rsvp@adst.keio.ac.jp Tel: (020) 7629 3577 Fax: (020) 7629 3588
Media Inquiries: Juli Morizawa (Ms), Akiko Kurata (Ms)
Office of Communications and Public Relations, Keio University, Japan
Email: m-koho@adst.keio.ac.jp Tel: +81-3-5427-1541 Fax: +81-3-5441-7640
Meeting information
“Frontiers of Neuroscience” April 27 (3 p.m. to 6 p.m.) at UCL’s Cruciform Lecture Theatre 2, Gower Street, London, UK.
Friday, April 13, 2007
Frontiers of Neuroscience - Major advancements in medical research and their applications
hosted by
Keio University, Japan
University College London, UK and Japan Society for the Promotion of Science
Friday April 27, 2007
3:00-6:00pm Entry Free Cruciform Lecture Theatre 2, UCL
Gower Street, London WC1
It is with great pleasure that Keio University, University College London, and Japan Society for the Promotion of Science (JSPS) invite you to the first Keio University 150th Anniversary International Symposium on “Frontiers of Neuroscience”.
Keio University is the oldest modern comprehensive university in Japan and will celebrate its 150th anniversary in 2008. It takes pride in having led Japanese society through innovations in both research and education from its earliest years when founder Yukichi Fukuzawa, who travelled to Europe as early as 1862, became convinced that Japan should transform itself through the introduction of western learning. In reaching this important milestone in its history, Keio is redoubling its commitment to strengthening its international profile and enhancing its global activities. To advance this endeavor, Keio has organized this symposium to highlight the university’s School of Medicine, renowned in Japan for its world-class and cutting-edge research and education, and has invited two of its distinguished academic members to participate.
Today, both the UK and Japan face the daunting reality of having become rapidly aging societies, largely as a result of major advancements in medical research and their applications. It is therefore timely and relevant for leading researchers in both countries to cooperate and share the results of their respective cutting-edge research activities in this field. It is a great pleasure for Keio University to co-host this event with University College London, the institution that introduced systematic medical education to England, and to welcome two of its leading professors as participants. The symposium will provide an opportunity to exchange current knowledge and research outcomes between UK and Japan at the highest level, which will be of interest both to academic experts and the general public.
This symposium will also commemorate the launch of the Keio University London Office, established in alliance with the JSPS London Office, a Japanese non-governmental organization committed to promoting bottom-up UK-Japan research collaboration. It is anticipated that this event will be the first of many joint activities advancing UK-Japan relations stimulated by the new partnership.
Speakers (In alphabetical order)
Professor Richard SJ Frackowiak
Vice-Provost (Special Projects)
Wellcome Department of Imaging Neuroscience, Institute of Neurology
University College London
Professor Hideyuki Okano
Department of Physiology
Keio University School of Medicine
Professor Masato Yasui
Professor and Chair, Department of Pharmacology
Keio University School of Medicine, Tokyo Japan
Professor Semir Zeki
Wellcome Department of Imaging Neuroscience
University College London
Programme
15:00-15:10 Opening address - Keio President Yuichiro Anzai
15:10-15:15 Introduction to the symposium - Professor Hideyuki Okano
15:15-15:40 "Modern Human Brain Imaging: structure-function correlations" Professor Richard Frackowiak
15:40-16:05 "Water Neurobiology: potential roles of water channel, aquaporin" Professor Masato Yasui
16:05-16:30 "Challenges toward Regeneration of the Damaged Central Nervous System" Professor Hideyuki Okano
16:30-16:55 " The Many Consciousnesses of the Brain " Professor Semir Zeki
16:55-17:15 Break
17:15-17:45 Panel discussion and Q& A
Chair: Professor Hideyuki Okano
Panelists:
President Yuichiro Anzai
Professor Richard SJ Frackowiak
Dr. Yukio Nishizawa, Research Director, Eisai London Research Laboratories
Professor Masato Yasui
Professor Semir Zeki
17:45-17:50 Closing address Ms. Yuko Furukawa, Director, JSPS London Office
-----------------------------------------------------------
18:00-19:30 Reception at the South Cloisters
While serving as a forum for advanced academic exchange, the program is designed to be accessible to all audiences. Admission is free of charge and open to the public.
Advance registration is required: sympo-rsvp@adst.keio.ac.jp (English and Japanese)
Event details: http://keio150.jp/english/events/2007/20070427e.html
For more articles and topics visit- www.medianowonline.com
hosted by
Keio University, Japan
University College London, UK and Japan Society for the Promotion of Science
Friday April 27, 2007
3:00-6:00pm Entry Free Cruciform Lecture Theatre 2, UCL
Gower Street, London WC1
It is with great pleasure that Keio University, University College London, and Japan Society for the Promotion of Science (JSPS) invite you to the first Keio University 150th Anniversary International Symposium on “Frontiers of Neuroscience”.
Keio University is the oldest modern comprehensive university in Japan and will celebrate its 150th anniversary in 2008. It takes pride in having led Japanese society through innovations in both research and education from its earliest years when founder Yukichi Fukuzawa, who travelled to Europe as early as 1862, became convinced that Japan should transform itself through the introduction of western learning. In reaching this important milestone in its history, Keio is redoubling its commitment to strengthening its international profile and enhancing its global activities. To advance this endeavor, Keio has organized this symposium to highlight the university’s School of Medicine, renowned in Japan for its world-class and cutting-edge research and education, and has invited two of its distinguished academic members to participate.
Today, both the UK and Japan face the daunting reality of having become rapidly aging societies, largely as a result of major advancements in medical research and their applications. It is therefore timely and relevant for leading researchers in both countries to cooperate and share the results of their respective cutting-edge research activities in this field. It is a great pleasure for Keio University to co-host this event with University College London, the institution that introduced systematic medical education to England, and to welcome two of its leading professors as participants. The symposium will provide an opportunity to exchange current knowledge and research outcomes between UK and Japan at the highest level, which will be of interest both to academic experts and the general public.
This symposium will also commemorate the launch of the Keio University London Office, established in alliance with the JSPS London Office, a Japanese non-governmental organization committed to promoting bottom-up UK-Japan research collaboration. It is anticipated that this event will be the first of many joint activities advancing UK-Japan relations stimulated by the new partnership.
Speakers (In alphabetical order)
Professor Richard SJ Frackowiak
Vice-Provost (Special Projects)
Wellcome Department of Imaging Neuroscience, Institute of Neurology
University College London
Professor Hideyuki Okano
Department of Physiology
Keio University School of Medicine
Professor Masato Yasui
Professor and Chair, Department of Pharmacology
Keio University School of Medicine, Tokyo Japan
Professor Semir Zeki
Wellcome Department of Imaging Neuroscience
University College London
Programme
15:00-15:10 Opening address - Keio President Yuichiro Anzai
15:10-15:15 Introduction to the symposium - Professor Hideyuki Okano
15:15-15:40 "Modern Human Brain Imaging: structure-function correlations" Professor Richard Frackowiak
15:40-16:05 "Water Neurobiology: potential roles of water channel, aquaporin" Professor Masato Yasui
16:05-16:30 "Challenges toward Regeneration of the Damaged Central Nervous System" Professor Hideyuki Okano
16:30-16:55 " The Many Consciousnesses of the Brain " Professor Semir Zeki
16:55-17:15 Break
17:15-17:45 Panel discussion and Q& A
Chair: Professor Hideyuki Okano
Panelists:
President Yuichiro Anzai
Professor Richard SJ Frackowiak
Dr. Yukio Nishizawa, Research Director, Eisai London Research Laboratories
Professor Masato Yasui
Professor Semir Zeki
17:45-17:50 Closing address Ms. Yuko Furukawa, Director, JSPS London Office
-----------------------------------------------------------
18:00-19:30 Reception at the South Cloisters
While serving as a forum for advanced academic exchange, the program is designed to be accessible to all audiences. Admission is free of charge and open to the public.
Advance registration is required: sympo-rsvp@adst.keio.ac.jp (English and Japanese)
Event details: http://keio150.jp/english/events/2007/20070427e.html
For more articles and topics visit- www.medianowonline.com
Thursday, April 12, 2007
Punish the rich- games of experimental economics We’re more likely to punish the rich than the poor, at least in games of experimental economics. The strategy is emotionally driven and the results suggest that human social behaviour is influenced by egalitarian motives.
James H. Fowler and colleagues set up a game where players were randomly allocated different sums of money, and were then able to ‘reward’ or ‘punish’ others by giving or taking money away. The richest players were penalized the hardest, whereas the poorest players were penalized the least.
The results show that people will reduce and increase others’ incomes at a personal cost, even when there is no cooperative behaviour to be reinforced. Their decisions are emotionally led, and the size and frequency of income alternations are strongly influenced by inequality — the pattern of punishments is designed to minimize inequality between the richest and poorest. The study suggests that egalitarian motives affect whether or not we donate cash to others, and this may be an important factor underlying the evolution of cooperation in humans.
CONTACT
James H. Fowler (University of California San Diego, La Jolla, CA, USA)
Tel: +1 858 534 6807; E-mail: jhfowler@ucsd.edu
For more articles and topics go to www.medianowonline.com
James H. Fowler and colleagues set up a game where players were randomly allocated different sums of money, and were then able to ‘reward’ or ‘punish’ others by giving or taking money away. The richest players were penalized the hardest, whereas the poorest players were penalized the least.
The results show that people will reduce and increase others’ incomes at a personal cost, even when there is no cooperative behaviour to be reinforced. Their decisions are emotionally led, and the size and frequency of income alternations are strongly influenced by inequality — the pattern of punishments is designed to minimize inequality between the richest and poorest. The study suggests that egalitarian motives affect whether or not we donate cash to others, and this may be an important factor underlying the evolution of cooperation in humans.
CONTACT
James H. Fowler (University of California San Diego, La Jolla, CA, USA)
Tel: +1 858 534 6807; E-mail: jhfowler@ucsd.edu
For more articles and topics go to www.medianowonline.com
Photochemistry: Quantum tricks in photosynthesis
The weird world of quantum physics meets biology with the discovery that quantum mechanical effects appear to play a role in photosynthesis.
Graham R. Fleming and colleagues used spectroscopy to study what happens inside a bacteriochlorophyll complex, and detected a ‘quantum beating’. The effect occurs when light-induced excitations in the complex meet and interfere constructively — much like the interactions that occur between the ripples formed by throwing stones into a pond.
Photosynthesis is the all-important process that transforms light, carbon dioxide and water into chemical energy in plants and some bacteria. This wavelike characteristic of this energy transfer process can explain its extreme efficiency, in that vast areas of phase space can be sampled effectively to find the most efficient path for energy transfer.
CONTACT
Graham R. Fleming (Lawrence Berkeley National Laboratory & University of California, Berkeley, CA, USA)
Tel: +1 510 643 2735; E-mail: fleming@cchem.berkeley.edu or grfleming@lbl.gov
Roseanne J. Sension (University of Michigan, Ann Arbor, MI, USA) N&V author
Tel: +1 734 763 6074; E-mail: rsension@umich.edu
For more topics and articles go to www.medianowonline.com
The weird world of quantum physics meets biology with the discovery that quantum mechanical effects appear to play a role in photosynthesis.
Graham R. Fleming and colleagues used spectroscopy to study what happens inside a bacteriochlorophyll complex, and detected a ‘quantum beating’. The effect occurs when light-induced excitations in the complex meet and interfere constructively — much like the interactions that occur between the ripples formed by throwing stones into a pond.
Photosynthesis is the all-important process that transforms light, carbon dioxide and water into chemical energy in plants and some bacteria. This wavelike characteristic of this energy transfer process can explain its extreme efficiency, in that vast areas of phase space can be sampled effectively to find the most efficient path for energy transfer.
CONTACT
Graham R. Fleming (Lawrence Berkeley National Laboratory & University of California, Berkeley, CA, USA)
Tel: +1 510 643 2735; E-mail: fleming@cchem.berkeley.edu or grfleming@lbl.gov
Roseanne J. Sension (University of Michigan, Ann Arbor, MI, USA) N&V author
Tel: +1 734 763 6074; E-mail: rsension@umich.edu
For more topics and articles go to www.medianowonline.com
Smart materials: A light touch (pp 778-781; N&V)
Researchers have developed crystals that will change their shape repeatedly when exposed to different types of light. The discovery may aid the development of light-driven actuators — mechanical devices that move or control things.
The molecular crystals, developed by Masahiro Irie and colleagues, are based on a particular type of light-absorbing molecule and range from 10 to 100 micrometres in size. When ultraviolet light is shone on one type of crystal, it changes shape from a square to a lozenge. But when the same crystal is exposed to visible light, it undergoes another mechanical deformation to change back to its original form. When put in the spotlight, a rod-shaped crystal of the material attached to a surface will even oblige and use this effect to 'bat' away a micrometre-sized gold particle.
The system is stable and responds quickly, within microseconds. Previous light-responsive systems, made from liquid crystals or polymer gels, can change shape but the effect takes seconds or longer and the deformed states are unstable. And the beauty of using light as a stimulus is that it offers the intriguing prospect of actuators that can be operated remotely.
CONTACT
Masahiro Irie (Rikkyo University, Tokyo, Japan)
Tel: +81 3 3985 2397; E-mail: irie@cstf.kyushu-u.ac.jp
J. Michael McBride (Yale University, New Haven, CT, USA) N&V author
Tel: +1 203 432 3926; E-mail: j.mcbride@yale.edu
For more articles and topics go to www.medianowonline.com
Researchers have developed crystals that will change their shape repeatedly when exposed to different types of light. The discovery may aid the development of light-driven actuators — mechanical devices that move or control things.
The molecular crystals, developed by Masahiro Irie and colleagues, are based on a particular type of light-absorbing molecule and range from 10 to 100 micrometres in size. When ultraviolet light is shone on one type of crystal, it changes shape from a square to a lozenge. But when the same crystal is exposed to visible light, it undergoes another mechanical deformation to change back to its original form. When put in the spotlight, a rod-shaped crystal of the material attached to a surface will even oblige and use this effect to 'bat' away a micrometre-sized gold particle.
The system is stable and responds quickly, within microseconds. Previous light-responsive systems, made from liquid crystals or polymer gels, can change shape but the effect takes seconds or longer and the deformed states are unstable. And the beauty of using light as a stimulus is that it offers the intriguing prospect of actuators that can be operated remotely.
CONTACT
Masahiro Irie (Rikkyo University, Tokyo, Japan)
Tel: +81 3 3985 2397; E-mail: irie@cstf.kyushu-u.ac.jp
J. Michael McBride (Yale University, New Haven, CT, USA) N&V author
Tel: +1 203 432 3926; E-mail: j.mcbride@yale.edu
For more articles and topics go to www.medianowonline.com
Cancer: Genes set scene for metastasis
Biologists have identified a set of genes expressed in human breast cancer cells that work together to remodel the vasculature at the site of the primary tumour and that also promote the spread of cancer to the lungs. The finding helps to explain how cancer metastasis can occur and highlights targets for therapeutic treatment.
Metastasis is the leading cause of mortality in cancer patients. A number of genes are already known to contribute to the spread of breast cancer cells to the lungs. But Joan Massagué and colleagues now show how four genes cooperate to promote the formation of new tumour blood vessels, the release of cancer cells into the bloodstream, and the penetration of tumour cells from the bloodstream into the lung.
The gene set comprises EREG, MMP1, MMP2 and COX2; drug combinations that target more than one of these components may prove useful for treating metastatic breast cancer.
CONTACT
Joan M Massague (Memorial Sloan-Kettering Cancer Center, Howard Hughes Medical Institute, New York, NY, USA)
Please contact:
Esther Napolitano (Public Affairs, Memorial Sloan-Kettering Cancer Center, New York, NY, USA)
Tel: +1 646 227 3139; E-mail: napolite@mskcc.org
Gerhard Christofori (University of Basel, Switzerland) N&V author
Tel: +41 61 267 3562 E-mail: gerhard.christofori@unibas.ch
Cancer: Genes linked to chemotherapy response
Scientists have identified a number of genes in lung cancer cells which, when downregulated, make the cancer cells especially vulnerable to a type of chemotherapy. The study highlights a new way to screen for alterations in cancer cells that make them specifically sensitive to therapeutics, so that treatment may leave normal tissue relatively unharmed.
Michael A. White and colleagues used a genome-wide RNA interference screen to identify 87 genes that are involved in the response of cancer cells to paclitaxel. Reducing the expression of a number of these genes sensitizes lung cancer cells to paclitaxel at concentrations 1,000-fold lower than otherwise needed for a significant response. Some of the identified genes are already targets of currently available compounds and could be tested for responses to combinations of drugs, whereas others could be new therapeutic targets.
CONTACT
Michael A. White (University of Texas Southwestern Medical Center, Dallas, TX, USA)
Tel: +1 214 648 2861; E-mail: michael.white@utsouthwestern.edu
For more articles and topics go to www.medianowonline.com
Biologists have identified a set of genes expressed in human breast cancer cells that work together to remodel the vasculature at the site of the primary tumour and that also promote the spread of cancer to the lungs. The finding helps to explain how cancer metastasis can occur and highlights targets for therapeutic treatment.
Metastasis is the leading cause of mortality in cancer patients. A number of genes are already known to contribute to the spread of breast cancer cells to the lungs. But Joan Massagué and colleagues now show how four genes cooperate to promote the formation of new tumour blood vessels, the release of cancer cells into the bloodstream, and the penetration of tumour cells from the bloodstream into the lung.
The gene set comprises EREG, MMP1, MMP2 and COX2; drug combinations that target more than one of these components may prove useful for treating metastatic breast cancer.
CONTACT
Joan M Massague (Memorial Sloan-Kettering Cancer Center, Howard Hughes Medical Institute, New York, NY, USA)
Please contact:
Esther Napolitano (Public Affairs, Memorial Sloan-Kettering Cancer Center, New York, NY, USA)
Tel: +1 646 227 3139; E-mail: napolite@mskcc.org
Gerhard Christofori (University of Basel, Switzerland) N&V author
Tel: +41 61 267 3562 E-mail: gerhard.christofori@unibas.ch
Cancer: Genes linked to chemotherapy response
Scientists have identified a number of genes in lung cancer cells which, when downregulated, make the cancer cells especially vulnerable to a type of chemotherapy. The study highlights a new way to screen for alterations in cancer cells that make them specifically sensitive to therapeutics, so that treatment may leave normal tissue relatively unharmed.
Michael A. White and colleagues used a genome-wide RNA interference screen to identify 87 genes that are involved in the response of cancer cells to paclitaxel. Reducing the expression of a number of these genes sensitizes lung cancer cells to paclitaxel at concentrations 1,000-fold lower than otherwise needed for a significant response. Some of the identified genes are already targets of currently available compounds and could be tested for responses to combinations of drugs, whereas others could be new therapeutic targets.
CONTACT
Michael A. White (University of Texas Southwestern Medical Center, Dallas, TX, USA)
Tel: +1 214 648 2861; E-mail: michael.white@utsouthwestern.edu
For more articles and topics go to www.medianowonline.com
Monday, April 09, 2007
Herbal supplement may help treat recurrent bladder infections
Washington, Apr 9 -An herbal extract that is sold in
health food stores and promoted as an allergy and fat loss aid
may improve treatment of bladder infections when it is taken
with antibiotics, research suggests.
Some 90 per cent of bladder infections are caused by E.
coli bacteria. They affect women four times more often than
men, sometimes recurring over and over.
The bladder is lined with small pouches that allow it to
stretch as it fills. Researchers at Duke University reported
in yesterday's online edition of Nature Medicine that some
bacteria were able to hide in those pouches, escaping the
antibiotics used to treat the infection.
In tests in mice, the extract forskolin can cause the
pouches to kick out the bacteria, allowing antibiotics to
kill them, said the lead researcher, microbiologist Soman N.
Abraham. Forskolin is derived from the Indian coleus plant.
"If we combine this with antibiotics we would be in a
very good position to eradicate urinary tract infection," he
said in a telephone interview.
In the experiments, forskolin was injected into some
mice and placed directly into the bladders in others, Abraham
said.
The extract is available in health food stores and some
people take it by mouth as a supplement, he said. It is
promoted as a treatment for allergies, breathing problems and
even fat loss.
That availability does "absolutely not" mean people
should attempt to treat themselves for bladder infections,
Abraham said.
Washington, Apr 9 -An herbal extract that is sold in
health food stores and promoted as an allergy and fat loss aid
may improve treatment of bladder infections when it is taken
with antibiotics, research suggests.
Some 90 per cent of bladder infections are caused by E.
coli bacteria. They affect women four times more often than
men, sometimes recurring over and over.
The bladder is lined with small pouches that allow it to
stretch as it fills. Researchers at Duke University reported
in yesterday's online edition of Nature Medicine that some
bacteria were able to hide in those pouches, escaping the
antibiotics used to treat the infection.
In tests in mice, the extract forskolin can cause the
pouches to kick out the bacteria, allowing antibiotics to
kill them, said the lead researcher, microbiologist Soman N.
Abraham. Forskolin is derived from the Indian coleus plant.
"If we combine this with antibiotics we would be in a
very good position to eradicate urinary tract infection," he
said in a telephone interview.
In the experiments, forskolin was injected into some
mice and placed directly into the bladders in others, Abraham
said.
The extract is available in health food stores and some
people take it by mouth as a supplement, he said. It is
promoted as a treatment for allergies, breathing problems and
even fat loss.
That availability does "absolutely not" mean people
should attempt to treat themselves for bladder infections,
Abraham said.
IT IS A DOG STORY
Scientists First to Isolate a Single Gene Common to All Small Dogs
From the smallest Chihuahua to the largest Great Dane, dogs dramatically vary in size, much more than most other animals. Now scientists have discovered a genetic basis for this diversity.
A new study published in research journal Science reveals a genetic marker that may determine whether dogs are big or small, and helps answer a burning question in genetics -- how could dogs as a species have such a tremendous variation in size?
"This study is a major milestone in canine genetics, made possible by the help of thousands of dog owners around the world. Together with a team of leading international researchers, we have precisely located the major gene that produces our miniature breeds," said co-author Paul G. Jones, PhD, a genetics researcher at Mars -- a world leader in pet care that has been researching canine genetic science for the last seven years.
Dogs were one of the earliest animals to be domesticated more than 15,000 years ago, although people and wolves have coexisted for some 400,000 years. While all dogs originated from wolves, which are of a fairly standard size and appearance, modern dog breeds display a wide diversity of traits, including size. The genetic origin of this diversity has baffled scientists, who have been trying to explain how and why size difference occurred so rapidly in dogs. It is now thought that a change in the gene detailed in the published paper resulted in the appearance of small dogs in the population many thousands of years ago. It is likely that people soon saw the benefits of smaller dogs, for example for protecting food stores from vermin or catching small game. This further strengthened the bond between people and dogs and led to increasing popularity of smaller dogs as companions.
The international team of researchers -- ranging from scientists at the National Human Genome Research Institute, Cornell and other leading universities in the U.S. to Mars scientists in the United Kingdom -- used 3,200 dog DNA samples provided by Mars Incorporated, which holds the most comprehensive canine genetic database in the world. This has been built up with the help of pet owners who consent to their pets providing saliva and blood samples for the database. Mars' genetic data allowed the study to fill the gap between giant and miniature breeds ensuring coverage across the entire range of sizes of breeds we have today.
"These findings are just the tip of the iceberg in canine genetics," Jones said. "We are well on our way to identifying additional genes that can provide valuable insights into our pets."
With the dog genome now fully mapped, scientists are discovering a range of potential benefits of DNA-based information on man's best friend.
"The ability to isolate a specific genetic marker in such a quick and effective manner has tremendous implications for the future," Jones said. "Applications of this cutting-edge science could be used to develop products that will benefit the health of pets -- for example, developing individualized preventative care plans for dogs that are susceptible to certain diseases will help pet owners and veterinarians. In addition, genetic information about size and behavioral traits, such as trainability and temperament could also help veterinarians identify the most lifestyle-appropriate pet for an owner. "
Dog Facts
Dogs have one of the widest variations in size of any species. The adult bodyweights of the largest breeds are up to 70 times more than those of the smallest breeds. According to the American Kennel Club, in 2006 the most popular large-breed dogs in the USA were the Labrador Retriever, the German Shepherd Dog and Golden Retrievers; the most popular small-breed dogs were Yorkshire Terriers, Dachshunds and Shih Tzus.
FOR OTHER TOPICS PLEASE VISIT OUR PORTAL www.medianowonline.com
METHODS : Enrichment of metabolites with chemical probes
A general strategy for enriching various classes of metabolites directly from biological samples is described.The method allows researchers to profile small molecule metabolites that are difficult to detect with more conventional discovery-based methods.
The proteomics community has greatly benefited from chemical enrichment methods allowing the targeted isolation of proteins with similar functional or structural properties. The ‘metabolome,’ or entire spectrum of small molecules found in an organism, is even greater than the proteome in terms of numbers and chemical complexity. Benjamin Cravatt and colleagues reasoned that metabolomics researchers would therefore also benefit from targeted chemical enrichment strategies.
The authors synthesized chemical probes to target specific functional groups on small molecules. The probes were attached to a solid bead for easy isolation of the captured small molecules. The captured metabolites were then released from the probe and analyzed by liquid chromatography-mass spectrometry. They demonstrated that the method was able to isolate and profile low mass and polar small molecules, which are usually missed with conventional analysis without enrichment.
Author contact:
Benjamin Cravatt (The Scripps Research Institute, La Jolla, CA, USA)
Tel: +1 858 784 8633; E-mail: cravatt@scripps.edu
for other topics please visit our portal www.medianowonline.com
A general strategy for enriching various classes of metabolites directly from biological samples is described.The method allows researchers to profile small molecule metabolites that are difficult to detect with more conventional discovery-based methods.
The proteomics community has greatly benefited from chemical enrichment methods allowing the targeted isolation of proteins with similar functional or structural properties. The ‘metabolome,’ or entire spectrum of small molecules found in an organism, is even greater than the proteome in terms of numbers and chemical complexity. Benjamin Cravatt and colleagues reasoned that metabolomics researchers would therefore also benefit from targeted chemical enrichment strategies.
The authors synthesized chemical probes to target specific functional groups on small molecules. The probes were attached to a solid bead for easy isolation of the captured small molecules. The captured metabolites were then released from the probe and analyzed by liquid chromatography-mass spectrometry. They demonstrated that the method was able to isolate and profile low mass and polar small molecules, which are usually missed with conventional analysis without enrichment.
Author contact:
Benjamin Cravatt (The Scripps Research Institute, La Jolla, CA, USA)
Tel: +1 858 784 8633; E-mail: cravatt@scripps.edu
for other topics please visit our portal www.medianowonline.com
IMMUNOLOGY : How one’s own DNA can cause autoimmunity
A study may shed light on the cause of immune activation associated with systemic lupus erythematosus (SLE) – the second most common autoimmune disease in humans.
Found more often in women than in men, SLE is associated with the abnormal production of antibodies that ‘attack’ normal molecules in the body, including a person’s own DNA. As a result, debilitating inflammation, including skin rashes, hypertension, arthritis, and kidney and nervous system problems, ensues. Anthony Coyle and colleagues studied a protein called HMGB1 that normally binds to DNA in the cell nucleus. HMGB1 is also found in blood plasma, where it can bind to DNA released from dying cells. In many SLE patients, such DNA is also often the target of ‘abnormal’ lupus antibodies. As a result, antibody–HMGB1–DNA protein complexes form. The new study by Coyle and colleagues finds that antibody–HMGB1–DNA complexes in blood plasma from SLE patients can stimulate immune cells to produce potent inflammatory proteins associated with autoimmunity.
By demonstrating a role for HMGB1 in SLE inflammation, Coyle and colleagues provide unique insight into the pathogenesis associated with increasingly prevalent autoimmune diseases such as SLE. However, whether blocking the inflammatory function of HMGB1 will help SLE patients remains a question for future investigation.
Author contact:
Anthony Coyle (MedImmune Inc, Gaithersberg, MD, USA)
Tel: +1 301 398 4520; E-mail: coylea@medimmune.com
for other topics please visit our portal www.medianowonline.com
A study may shed light on the cause of immune activation associated with systemic lupus erythematosus (SLE) – the second most common autoimmune disease in humans.
Found more often in women than in men, SLE is associated with the abnormal production of antibodies that ‘attack’ normal molecules in the body, including a person’s own DNA. As a result, debilitating inflammation, including skin rashes, hypertension, arthritis, and kidney and nervous system problems, ensues. Anthony Coyle and colleagues studied a protein called HMGB1 that normally binds to DNA in the cell nucleus. HMGB1 is also found in blood plasma, where it can bind to DNA released from dying cells. In many SLE patients, such DNA is also often the target of ‘abnormal’ lupus antibodies. As a result, antibody–HMGB1–DNA protein complexes form. The new study by Coyle and colleagues finds that antibody–HMGB1–DNA complexes in blood plasma from SLE patients can stimulate immune cells to produce potent inflammatory proteins associated with autoimmunity.
By demonstrating a role for HMGB1 in SLE inflammation, Coyle and colleagues provide unique insight into the pathogenesis associated with increasingly prevalent autoimmune diseases such as SLE. However, whether blocking the inflammatory function of HMGB1 will help SLE patients remains a question for future investigation.
Author contact:
Anthony Coyle (MedImmune Inc, Gaithersberg, MD, USA)
Tel: +1 301 398 4520; E-mail: coylea@medimmune.com
for other topics please visit our portal www.medianowonline.com
NEUROSCIENCE : Stabilization contra retardation
A paper published online in Nature Neuroscience this week explores the mechanisms underlying fragile X syndrome – the most common inherited form of mental retardation. This disorder is caused by loss of a protein, dubbed FMRP, which interacts with messenger RNAs. (mRNAs are the templates that a cell ‘reads’ to correctly build specific proteins.) The details of how FMRP affects mRNAs and protein synthesis, and how subtle misregulation in absence of FMRP causes mental retardation, are still unclear.
Claudia Bagni and Kirsten S. Dickson and colleagues now report that FMRP stabilizes the mRNA that encodes the protein PSD-95. PSD-95 is crucial for the structure and function of neural synapses. In the brains of mice lacking FMRP, the authors found that the PSD-95 mRNA was rapidly degraded. The level of PSD-95 protein was reduced especially in the hippocampus, a structure crucial for learning, memory and certain kinds of reasoning.
This work suggests an important role for mRNA stabilization in the circuit wiring and communication of nerve cell networks. Though it is unlikely that all fragile X mental retardation symptoms can be explained by instability of PSD-95 mRNA, it may well represent an important part of the disease mechanism.
Author contacts:
Claudia Bagni (Universita di Roma, Italy)
Tel: +39 06 501 703 213; E-mail: claudia.bagni@uniroma2.it
Kirsten S. Dickson (University of Edinburgh, UK)
E-mail: dickson.kris@gmail.com
for other topics visit our portal www.medianowonline.com
A paper published online in Nature Neuroscience this week explores the mechanisms underlying fragile X syndrome – the most common inherited form of mental retardation. This disorder is caused by loss of a protein, dubbed FMRP, which interacts with messenger RNAs. (mRNAs are the templates that a cell ‘reads’ to correctly build specific proteins.) The details of how FMRP affects mRNAs and protein synthesis, and how subtle misregulation in absence of FMRP causes mental retardation, are still unclear.
Claudia Bagni and Kirsten S. Dickson and colleagues now report that FMRP stabilizes the mRNA that encodes the protein PSD-95. PSD-95 is crucial for the structure and function of neural synapses. In the brains of mice lacking FMRP, the authors found that the PSD-95 mRNA was rapidly degraded. The level of PSD-95 protein was reduced especially in the hippocampus, a structure crucial for learning, memory and certain kinds of reasoning.
This work suggests an important role for mRNA stabilization in the circuit wiring and communication of nerve cell networks. Though it is unlikely that all fragile X mental retardation symptoms can be explained by instability of PSD-95 mRNA, it may well represent an important part of the disease mechanism.
Author contacts:
Claudia Bagni (Universita di Roma, Italy)
Tel: +39 06 501 703 213; E-mail: claudia.bagni@uniroma2.it
Kirsten S. Dickson (University of Edinburgh, UK)
E-mail: dickson.kris@gmail.com
for other topics visit our portal www.medianowonline.com
GENETICS : Amplification of oestrogen receptor gene in breast cancer
A fifth of breast tumours have extra copies of the gene encoding one form of the oestrogens receptor ESR1, suggests a study. A small-scale initial study shows that women treated with tamoxifen, which blocks the activity of the oestrogens receptor, survive longer if their tumour has this gene amplification.
Oestrogens receptor expression is one of the most important known factors in the development of breast cancer, and assessing its status is important for determining the use of anti-oestrogens receptor therapies like tamoxifen. Ronald Simon and colleagues examined more than 2,000 breast cancer samples for evidence of amplification of ESR1, and detected it in 20.6 % of the tumours. In a small follow-up study of 175 women with breast cancer who were being treated with tamoxifen, they found that women with the amplification survived longer than those who did not, even though the tumours in both groups of women expressed ESR1. The authors suggest that ESR1 amplification may identify a subgroup of breast cancers that would be particularly likely to respond to anti-oestrogens therapy.
Author contact:
Ronald Simon (University Medical Center Hamburg Eppendorf, Germany)
Tel: +49 42803 7214; E-mail: r.simon@uke.uni-hamburg.de
Natural genetic variant influencing rice grain weight
A study published in Nature Genetics this week identifies a gene that influences rice grain weight and yield. This is only the second such gene that has been found and functionally characterized, and is a step toward understanding and improving grain yield in crops.
Rice is a staple food, and the world’s most important cereal crop. Hong-Xuan Lin and colleagues examined two varieties of rice that exhibit significant differences in grain size, and mapped the gene responsible for this variation in size – GW2. The version of GW2 found in the large-grain variety of rice increased the width and weight of rice grains and increases grain yield per plant by nearly 20%, although the authors caution that its effect on grain yield needs to be further assessed in randomized blocks of plants in paddies.
Initial experiments also show that rice with the high-yield variant of GW2 has no reduction in cooking or eating quality, suggesting that it will be useful for high-yield crop breeding. GW2 encodes a protein that belongs to a family of enzymes that target other proteins for degradation, and the authors speculate that it could affect grain size by regulating the cell division cycle.
Author contact:
Hong-Xuan Lin (Shanghai Institute for Biological Sciences, China)
Tel: +86 21 5492 4129; E-mail: hxlin@sibs.ac.cn
for other topics visit our portal- www.medianowonline.com
A fifth of breast tumours have extra copies of the gene encoding one form of the oestrogens receptor ESR1, suggests a study. A small-scale initial study shows that women treated with tamoxifen, which blocks the activity of the oestrogens receptor, survive longer if their tumour has this gene amplification.
Oestrogens receptor expression is one of the most important known factors in the development of breast cancer, and assessing its status is important for determining the use of anti-oestrogens receptor therapies like tamoxifen. Ronald Simon and colleagues examined more than 2,000 breast cancer samples for evidence of amplification of ESR1, and detected it in 20.6 % of the tumours. In a small follow-up study of 175 women with breast cancer who were being treated with tamoxifen, they found that women with the amplification survived longer than those who did not, even though the tumours in both groups of women expressed ESR1. The authors suggest that ESR1 amplification may identify a subgroup of breast cancers that would be particularly likely to respond to anti-oestrogens therapy.
Author contact:
Ronald Simon (University Medical Center Hamburg Eppendorf, Germany)
Tel: +49 42803 7214; E-mail: r.simon@uke.uni-hamburg.de
Natural genetic variant influencing rice grain weight
A study published in Nature Genetics this week identifies a gene that influences rice grain weight and yield. This is only the second such gene that has been found and functionally characterized, and is a step toward understanding and improving grain yield in crops.
Rice is a staple food, and the world’s most important cereal crop. Hong-Xuan Lin and colleagues examined two varieties of rice that exhibit significant differences in grain size, and mapped the gene responsible for this variation in size – GW2. The version of GW2 found in the large-grain variety of rice increased the width and weight of rice grains and increases grain yield per plant by nearly 20%, although the authors caution that its effect on grain yield needs to be further assessed in randomized blocks of plants in paddies.
Initial experiments also show that rice with the high-yield variant of GW2 has no reduction in cooking or eating quality, suggesting that it will be useful for high-yield crop breeding. GW2 encodes a protein that belongs to a family of enzymes that target other proteins for degradation, and the authors speculate that it could affect grain size by regulating the cell division cycle.
Author contact:
Hong-Xuan Lin (Shanghai Institute for Biological Sciences, China)
Tel: +86 21 5492 4129; E-mail: hxlin@sibs.ac.cn
for other topics visit our portal- www.medianowonline.com
CHEMICAL BIOLOGY :Chemical control of neural stem cells
Chemicals that regulate neurotransmitter signalling in neurons can also prevent neural stem cell proliferation, according to a paper in the May 2007 issue of Nature Chemical Biology. Neural stem cells are a potentially important therapeutic target for neurological diseases and brain tumours. However, very little is known about the potential for using small molecules to regulate neural stem cell differentiation and proliferation.
Using cultures of neural precursor cells, Peter B. Dirks and colleagues screened a chemical library for inhibitors of neural precursor cell proliferation. Within the ‘hits’ were a number of small molecules that are known to influence neurotransmitter signalling in neurons. These unexpected results indicate that neurotransmitter signalling pathways may also function in neural stem cells and raises the possibility of using existing drugs that regulate neurotransmitter signalling in the treatment of brain tumours.
Author contact:
Peter B. Dirks (The Hospital for Sick Children and University of Toronto, Canada)
Tel: +1 416 813 6426; E-mail: peter.dirks@sickkids.ca
Additional contact for comment on paper:
Mike Tyers, (Mount Sinai Hospital, Toronto, Canada)
Tel: +1 416 586 8371; E-mail: tyers@mshri.on.ca
for other topics visit our portal- www.medianowonline.com
Chemicals that regulate neurotransmitter signalling in neurons can also prevent neural stem cell proliferation, according to a paper in the May 2007 issue of Nature Chemical Biology. Neural stem cells are a potentially important therapeutic target for neurological diseases and brain tumours. However, very little is known about the potential for using small molecules to regulate neural stem cell differentiation and proliferation.
Using cultures of neural precursor cells, Peter B. Dirks and colleagues screened a chemical library for inhibitors of neural precursor cell proliferation. Within the ‘hits’ were a number of small molecules that are known to influence neurotransmitter signalling in neurons. These unexpected results indicate that neurotransmitter signalling pathways may also function in neural stem cells and raises the possibility of using existing drugs that regulate neurotransmitter signalling in the treatment of brain tumours.
Author contact:
Peter B. Dirks (The Hospital for Sick Children and University of Toronto, Canada)
Tel: +1 416 813 6426; E-mail: peter.dirks@sickkids.ca
Additional contact for comment on paper:
Mike Tyers, (Mount Sinai Hospital, Toronto, Canada)
Tel: +1 416 586 8371; E-mail: tyers@mshri.on.ca
for other topics visit our portal- www.medianowonline.com
Thursday, April 05, 2007
Algorithm for group success?
Want to know how to make your clique, group or organization last? A new algorithm can help you do just that.
Tamás Vicsek and colleagues studied the patterns of information exchange within two groups of individuals — collaborating scientists and mobile phone users — over time. From this, they devised an algorithm to let them study how information exchange affects group stability.
Small groups, they report, have a few strong relationships at their core. And as long as these persist, the clique remains. But the strategy doesn’t work for large communities, where change seems a good thing. Continuous change helps large groups to remain stable, and over time, nearly all members are exchanged.
The findings help shed light on the basic relationships behind community evolution, and offer insights into the fundamental differences between the dynamics of small groups and large institutions.
CONTACT
Tamás Vicsek (Eötvös Loránd University, Budapest, Hungary)
Tel: +36 1 372 2755; E-mail: vicsek@angel.elte.hu
Want to know how to make your clique, group or organization last? A new algorithm can help you do just that.
Tamás Vicsek and colleagues studied the patterns of information exchange within two groups of individuals — collaborating scientists and mobile phone users — over time. From this, they devised an algorithm to let them study how information exchange affects group stability.
Small groups, they report, have a few strong relationships at their core. And as long as these persist, the clique remains. But the strategy doesn’t work for large communities, where change seems a good thing. Continuous change helps large groups to remain stable, and over time, nearly all members are exchanged.
The findings help shed light on the basic relationships behind community evolution, and offer insights into the fundamental differences between the dynamics of small groups and large institutions.
CONTACT
Tamás Vicsek (Eötvös Loránd University, Budapest, Hungary)
Tel: +36 1 372 2755; E-mail: vicsek@angel.elte.hu
Atom spectroscopy: The great electron escape
Researchers have 'observed' electrons being stripped away from atoms by intense light fields. The technique used should offer control over, and provide insights into, the dynamics of electrons inside atoms and molecules.
Given enough energy, electrons can ‘tunnel’ through the potential barrier that normally binds them to their nucleus, and escape. Ferenc Krausz and colleagues have now ‘seen’ this light-induced electron tunnelling happen in real time on the attosecond — that’s one billionth of one billionth of a second — timescale.
The team ionized neon atoms with ultrafast far-ultraviolet pulses, and then probed them with near-infrared pulses. From the observed spectra, they were then able to reconstruct the electron tunnelling.
CONTACT
Ferenc Krausz (Max-Planck-Institut für Quantenoptik, Garching, Germany)
Tel: +49 89 3290 5602; E-mail: ferenc.krausz@mpq.mpg.de
Jonathan P. Marangos (Imperial College London, UK) N&V author
Tel: +44 20 7594 7857; E-mail: j.marangos@imperial.ac.uk
Researchers have 'observed' electrons being stripped away from atoms by intense light fields. The technique used should offer control over, and provide insights into, the dynamics of electrons inside atoms and molecules.
Given enough energy, electrons can ‘tunnel’ through the potential barrier that normally binds them to their nucleus, and escape. Ferenc Krausz and colleagues have now ‘seen’ this light-induced electron tunnelling happen in real time on the attosecond — that’s one billionth of one billionth of a second — timescale.
The team ionized neon atoms with ultrafast far-ultraviolet pulses, and then probed them with near-infrared pulses. From the observed spectra, they were then able to reconstruct the electron tunnelling.
CONTACT
Ferenc Krausz (Max-Planck-Institut für Quantenoptik, Garching, Germany)
Tel: +49 89 3290 5602; E-mail: ferenc.krausz@mpq.mpg.de
Jonathan P. Marangos (Imperial College London, UK) N&V author
Tel: +44 20 7594 7857; E-mail: j.marangos@imperial.ac.uk
Earth sciences: A salty solution
A new modelling study offers an elegant explanation for a curious anomaly seen in the carbon and sulphur isotope records of the Early Cretaceous period.
In modern-day sediments, the rates of pyrite (iron sulphide) and carbon-based organic matter burial are positively related. But during the Early Cretaceous period, which began approximately 140 million years ago, they appear to be negatively related — a relationship that has, until now, been difficult to explain.
Ulrich G. Wortmann and Boris M. Chernyavsky show that this puzzling relationship could be due to the deposition of evaporites — mineral sediments that precipitate from water as it evaporates — on the ocean floor as South Africa and South America moved apart and the South Atlantic Ocean basin formed. The evaporites contain sulphate, so their production removed sulphate from the surrounding waters. Enough, the model suggests, to reduce significantly the rate at which organisms in marine sediments formed pyrite and broke down organic matter, thus explaining the negative relationship between the amount of pyrite and organic matter buried in marine sediments at this time.
Evaporite deposition may have had a similar effect at other times in Earth’s history, and so may explain other changes in carbon and sulphur cycling. These are important to understand because alterations in these cycles can have a direct effect on atmospheric oxygen levels.
CONTACT
Ulrich G. Wortmann (University of Toronto, Canada)
Tel: +1 416 978 7084; E-mail: uli.wortmann@utoronto.ca
A new modelling study offers an elegant explanation for a curious anomaly seen in the carbon and sulphur isotope records of the Early Cretaceous period.
In modern-day sediments, the rates of pyrite (iron sulphide) and carbon-based organic matter burial are positively related. But during the Early Cretaceous period, which began approximately 140 million years ago, they appear to be negatively related — a relationship that has, until now, been difficult to explain.
Ulrich G. Wortmann and Boris M. Chernyavsky show that this puzzling relationship could be due to the deposition of evaporites — mineral sediments that precipitate from water as it evaporates — on the ocean floor as South Africa and South America moved apart and the South Atlantic Ocean basin formed. The evaporites contain sulphate, so their production removed sulphate from the surrounding waters. Enough, the model suggests, to reduce significantly the rate at which organisms in marine sediments formed pyrite and broke down organic matter, thus explaining the negative relationship between the amount of pyrite and organic matter buried in marine sediments at this time.
Evaporite deposition may have had a similar effect at other times in Earth’s history, and so may explain other changes in carbon and sulphur cycling. These are important to understand because alterations in these cycles can have a direct effect on atmospheric oxygen levels.
CONTACT
Ulrich G. Wortmann (University of Toronto, Canada)
Tel: +1 416 978 7084; E-mail: uli.wortmann@utoronto.ca
Geology: Geomagnetic data captured in crystals
Researchers have used silicate crystals to determine the strength of the Earth’s geomagnetic field around 3.2 billion years ago. Their findings should help to shed light on the evolution of the Earth’s deep interior, surface environment and atmosphere.
John A. Tarduno and colleagues studied silicate crystals from well preserved igneous rocks found in South Africa’s Archaean Kaapvaal craton. The crystals contain minute magnetic inclusions, and the team calculate that 3.2 billion years ago, the Earth’s geomagnetic field strength was within fifty per cent of the present-day value. This means that there was probably a viable magnetosphere to shelter the planet from solar wind erosion at that time.
Little is known about the strength of the Earth’s geomagnetic field before 2.8 billion years ago, so the new data offer a welcome insight into the Earth’s geomagnetic history.
CONTACT
John A. Tarduno (University of Rochester, NY, USA)
Tel: +1 585 275 5713; E-mail: john@earth.rochester.edu
David J. Dunlop (University of Toronto, Canada) N&V author
Tel: +1 905 828 3968; E-mail: dunlop@physics.utoronto.ca
Researchers have used silicate crystals to determine the strength of the Earth’s geomagnetic field around 3.2 billion years ago. Their findings should help to shed light on the evolution of the Earth’s deep interior, surface environment and atmosphere.
John A. Tarduno and colleagues studied silicate crystals from well preserved igneous rocks found in South Africa’s Archaean Kaapvaal craton. The crystals contain minute magnetic inclusions, and the team calculate that 3.2 billion years ago, the Earth’s geomagnetic field strength was within fifty per cent of the present-day value. This means that there was probably a viable magnetosphere to shelter the planet from solar wind erosion at that time.
Little is known about the strength of the Earth’s geomagnetic field before 2.8 billion years ago, so the new data offer a welcome insight into the Earth’s geomagnetic history.
CONTACT
John A. Tarduno (University of Rochester, NY, USA)
Tel: +1 585 275 5713; E-mail: john@earth.rochester.edu
David J. Dunlop (University of Toronto, Canada) N&V author
Tel: +1 905 828 3968; E-mail: dunlop@physics.utoronto.ca
Microbiology: Antibiotic-resistant bacteria meet their match?
Researchers may have found a way of keeping drug-resistant bacteria in check — certain combinations of antibiotics favour the growth of non-resistant strains at the expense of resistant ones. The finding may help combat the spread of these microbes, as well as shed light on microbial ecology and evolution.
Antagonistic drug combinations, in which the drugs' cumulative effects are less than when they are given separately, show such effects, say Roy Kishony and colleagues. At sublethal concentrations, a mixture of doxycycline and ciprofloxacin preferentially selects for wild-type Escherichia coli bacteria over that of a doxycyline-resistant strain in a laboratory culture.
The finding is surprising and counter-intuitive, as the use of antibiotic drugs is responsible for the generation and selection of resistant bacterial pathogen strains. But this study shows that, with the right combinations and concentrations, non-resistant bacterial strains can be selected for.
CONTACT
Roy Kishony (Harvard Medical School, Boston, MA, USA)
Tel: +1 617 432 6390; E-mail: roy_kishony@hms.harvard.edu
Researchers may have found a way of keeping drug-resistant bacteria in check — certain combinations of antibiotics favour the growth of non-resistant strains at the expense of resistant ones. The finding may help combat the spread of these microbes, as well as shed light on microbial ecology and evolution.
Antagonistic drug combinations, in which the drugs' cumulative effects are less than when they are given separately, show such effects, say Roy Kishony and colleagues. At sublethal concentrations, a mixture of doxycycline and ciprofloxacin preferentially selects for wild-type Escherichia coli bacteria over that of a doxycyline-resistant strain in a laboratory culture.
The finding is surprising and counter-intuitive, as the use of antibiotic drugs is responsible for the generation and selection of resistant bacterial pathogen strains. But this study shows that, with the right combinations and concentrations, non-resistant bacterial strains can be selected for.
CONTACT
Roy Kishony (Harvard Medical School, Boston, MA, USA)
Tel: +1 617 432 6390; E-mail: roy_kishony@hms.harvard.edu
Planetary science: Winds of change
Variations in the radiation reflected from the surface of Mars are contributing to climate change on the planet, by causing increased dust transport and wind circulation. A study predicts that the planet has warmed by around 0.65 degrees Celsius from the 1970s to the 1990s, which may in part have caused the recent retreat of the southern polar ice cap.
The fraction of solar radiation reflected from an object is called its albedo — and on Mars, large areas on the surface show a contrast in brightness or darkness with the areas next to them, resulting in albedo patterns, which can change in appearance over time. These changes in brightness have been generally attributed to the presence of dust, but until now their effect on wind circulation and climate has not been clear.
Lori K. Fenton and colleagues present predictions from a Mars global circulation model which show that these changes are having a much larger than expected effect on climate. Large swaths of the surface have darkened over the past three decades as they were swept free of dust, leading to elevated air temperatures and increased wind stresses. This creates a positive feedback loop between dust erosion and albedo. The authors conclude that albedo variations interact with, and can in part drive, other climate-influencing processes on Mars, and should be considered as an important component in future atmospheric and climate studies of the planet.
CONTACT
Lori K. Fenton (Carl Sagan Center, NASA Ames Reserach Centre, Moffett Field, CA, USA)
Tel: +1 510 786 7199; E-mail: lfenton@carlsagancenter.org or fenton@mintz.arc.nasa.gov
Variations in the radiation reflected from the surface of Mars are contributing to climate change on the planet, by causing increased dust transport and wind circulation. A study predicts that the planet has warmed by around 0.65 degrees Celsius from the 1970s to the 1990s, which may in part have caused the recent retreat of the southern polar ice cap.
The fraction of solar radiation reflected from an object is called its albedo — and on Mars, large areas on the surface show a contrast in brightness or darkness with the areas next to them, resulting in albedo patterns, which can change in appearance over time. These changes in brightness have been generally attributed to the presence of dust, but until now their effect on wind circulation and climate has not been clear.
Lori K. Fenton and colleagues present predictions from a Mars global circulation model which show that these changes are having a much larger than expected effect on climate. Large swaths of the surface have darkened over the past three decades as they were swept free of dust, leading to elevated air temperatures and increased wind stresses. This creates a positive feedback loop between dust erosion and albedo. The authors conclude that albedo variations interact with, and can in part drive, other climate-influencing processes on Mars, and should be considered as an important component in future atmospheric and climate studies of the planet.
CONTACT
Lori K. Fenton (Carl Sagan Center, NASA Ames Reserach Centre, Moffett Field, CA, USA)
Tel: +1 510 786 7199; E-mail: lfenton@carlsagancenter.org or fenton@mintz.arc.nasa.gov
Neuroscience: A light-switch for brain cells
An elegant technique using light to control the activity of brain cells is described. By expressing a light-responsive membrane protein in neurons, researchers can inhibit neural activity on a millisecond timescale.
Karl Deisseroth and colleagues introduced NpHR — a light-driven chloride pump that occurs naturally in microorganisms known as archaea — into cultured mammalian neurons and brain tissue in the laboratory. Training light pulses of a particular wavelength onto these cells effectively inhibited neural activity. This builds on the authors’ previous work using the protein ChR2 — a light-responsive channel found in algae — to optically excite nerve cells with light of a different wavelength. By simultaneously expressing both membrane proteins in the muscle cells or motor neurons of the nematode worm Caenorhabditis elegans, the authors were able to control its locomotive behaviour — the worms stopped and started muscle contractions when yellow and blue lights were shone on them.
These findings demonstrate that light-responsive proteins can be used simultaneously to permit fast, bidirectional and reversible control over living neural circuits. They can also be used in conjunction with calcium imaging techniques and, together, provide a powerful tool for studying and manipulating brain activity with high precision.
CONTACTKarl Deisseroth (Stanford University, CA, USA)
Tel: +1 650 736 4325; E-mail: deissero@gmail.com
Michael Hausser (University College London, UK) N&V author
Tel: +44 207 679 6756; E-mail: m.hausser@ucl.ac.uk
An elegant technique using light to control the activity of brain cells is described. By expressing a light-responsive membrane protein in neurons, researchers can inhibit neural activity on a millisecond timescale.
Karl Deisseroth and colleagues introduced NpHR — a light-driven chloride pump that occurs naturally in microorganisms known as archaea — into cultured mammalian neurons and brain tissue in the laboratory. Training light pulses of a particular wavelength onto these cells effectively inhibited neural activity. This builds on the authors’ previous work using the protein ChR2 — a light-responsive channel found in algae — to optically excite nerve cells with light of a different wavelength. By simultaneously expressing both membrane proteins in the muscle cells or motor neurons of the nematode worm Caenorhabditis elegans, the authors were able to control its locomotive behaviour — the worms stopped and started muscle contractions when yellow and blue lights were shone on them.
These findings demonstrate that light-responsive proteins can be used simultaneously to permit fast, bidirectional and reversible control over living neural circuits. They can also be used in conjunction with calcium imaging techniques and, together, provide a powerful tool for studying and manipulating brain activity with high precision.
CONTACTKarl Deisseroth (Stanford University, CA, USA)
Tel: +1 650 736 4325; E-mail: deissero@gmail.com
Michael Hausser (University College London, UK) N&V author
Tel: +44 207 679 6756; E-mail: m.hausser@ucl.ac.uk
The discovery of America: The revolutionary claims of a dead historian
New evidence could rewrite the history of the discovery of America
Dr Alwyn Ruddock, a former reader in history at the University of London, was the world expert on John Cabot’s discovery voyages from Bristol to North America (1496-98). What she was said to have found out about these voyages looked set to re-write the history of the European discovery of America. Yet, when Dr Ruddock died in December 2005, having spent four decades researching this topic, she ordered the destruction of all her research.
In an article published in Historical Research, Alwyn Ruddock’s extraordinary claims are explored by Dr Evan Jones of the University of Bristol.
In Spring 2006, all Dr Ruddock’s research material was destroyed, in line with the instructions in her will. However, her correspondence with her intended publisher, the University of Exeter Press, survived. Using this correspondence Dr Jones has investigated the research that Dr Ruddock had worked on, and kept secret, for so many years.
‘To describe Alwyn Ruddock’s claims as revolutionary,’ said Dr Jones, ‘is not an exaggeration.’ Her apparent findings include information about how John Cabot persuaded Henry VII to support his voyages and why the explorer was able to win the backing of an influential Italian cleric: Fr. Giovanni Antonio de Carbonariis, an Augustinian friar who was also in charge of collecting the Pope’s taxes in England.
Dr Ruddock’s most exciting claims, however, involve John Cabot’s 1498 voyage to America . While the fate of this expedition has long been a mystery, Dr Ruddock appears to have found evidence of a long and complex exploration of the American coastline, which culminated in Cabot’s return to England in the spring of 1500, followed shortly by his death. During this voyage, Dr Ruddock suggests that Cabot explored a large section of the coastline of North America, claiming it for England in the process.
Dr Ruddock intended to reveal that while Cabot was sailing south down the coast of America his chief supporter, Fra Giovanni, was establishing a religious colony in Newfoundland. Having disembarked from his ship, the Dominus Nobiscum, Fra Giovanni apparently established a settlement and built a church. This church, the first to be built in North America, was named after the Augustinian church of San Giovanni a Carbonara in Naples.
Dr Jones said: ‘Ruddock’s claims about the 1498 voyage are perhaps the most exciting of all. For while we have long known that Fra Giovanni accompanied the expedition, along with some other “poor Italian friars”, nothing has been known of what happened to their mission. If Ruddock is right, it means that the remains of the only medieval church in North America may still lie buried under the modern town of Carbonear.’
Dr Ruddock’s claims are clearly extraordinary but are they all correct? This is an issue that remains, in large part, to be resolved. In his article, Dr Jones shows that in many cases Alwyn Ruddock’s claims can be substantiated by reference to previously unknown material. However, much remains to be done.
Dr Jones continued: ‘In publishing this article now my intent was to put into the public domain what appear to be the last vestiges of Dr Ruddock’s research. While her correspondence does not give all the answers, it does provide many clues that historians can use to investigate her claims. I also hope that the publication of this article might persuade people who possess knowledge of Dr Ruddock’s research to come forward. For it is clear from her correspondence that many people must possess useful knowledge, ranging from her ex-students at the British Library to the “old and historic families in Italy” who gave her access to their private archives.’
As to why Alwyn Ruddock should have chosen to have all her research destroyed on her death, Dr Jones confesses that he has no clear answers. In her obituary in the Guardian newspaper, it was suggested that she destroyed the first draft of her book ‘because it did not meet her exacting standards.’ This does not explain, however, why she wanted everything destroyed – including her microfilms, her photographs and the transcripts of the documents she used.
‘What is clear,’ said Dr Jones, ‘is that she had a great sense of possession for her work and she felt this gave her the moral right to take her secrets to the grave. But even if all the documents she claimed to have found do come to light eventually, the mystery of why she sought to suppress her own basic research may never be resolved.’
Associated links
http://www.bristol.ac.uk/news/2007/5333.html
http://www.blackwell-synergy.com/toc/hisr/0/0
New evidence could rewrite the history of the discovery of America
Dr Alwyn Ruddock, a former reader in history at the University of London, was the world expert on John Cabot’s discovery voyages from Bristol to North America (1496-98). What she was said to have found out about these voyages looked set to re-write the history of the European discovery of America. Yet, when Dr Ruddock died in December 2005, having spent four decades researching this topic, she ordered the destruction of all her research.
In an article published in Historical Research, Alwyn Ruddock’s extraordinary claims are explored by Dr Evan Jones of the University of Bristol.
In Spring 2006, all Dr Ruddock’s research material was destroyed, in line with the instructions in her will. However, her correspondence with her intended publisher, the University of Exeter Press, survived. Using this correspondence Dr Jones has investigated the research that Dr Ruddock had worked on, and kept secret, for so many years.
‘To describe Alwyn Ruddock’s claims as revolutionary,’ said Dr Jones, ‘is not an exaggeration.’ Her apparent findings include information about how John Cabot persuaded Henry VII to support his voyages and why the explorer was able to win the backing of an influential Italian cleric: Fr. Giovanni Antonio de Carbonariis, an Augustinian friar who was also in charge of collecting the Pope’s taxes in England.
Dr Ruddock’s most exciting claims, however, involve John Cabot’s 1498 voyage to America . While the fate of this expedition has long been a mystery, Dr Ruddock appears to have found evidence of a long and complex exploration of the American coastline, which culminated in Cabot’s return to England in the spring of 1500, followed shortly by his death. During this voyage, Dr Ruddock suggests that Cabot explored a large section of the coastline of North America, claiming it for England in the process.
Dr Ruddock intended to reveal that while Cabot was sailing south down the coast of America his chief supporter, Fra Giovanni, was establishing a religious colony in Newfoundland. Having disembarked from his ship, the Dominus Nobiscum, Fra Giovanni apparently established a settlement and built a church. This church, the first to be built in North America, was named after the Augustinian church of San Giovanni a Carbonara in Naples.
Dr Jones said: ‘Ruddock’s claims about the 1498 voyage are perhaps the most exciting of all. For while we have long known that Fra Giovanni accompanied the expedition, along with some other “poor Italian friars”, nothing has been known of what happened to their mission. If Ruddock is right, it means that the remains of the only medieval church in North America may still lie buried under the modern town of Carbonear.’
Dr Ruddock’s claims are clearly extraordinary but are they all correct? This is an issue that remains, in large part, to be resolved. In his article, Dr Jones shows that in many cases Alwyn Ruddock’s claims can be substantiated by reference to previously unknown material. However, much remains to be done.
Dr Jones continued: ‘In publishing this article now my intent was to put into the public domain what appear to be the last vestiges of Dr Ruddock’s research. While her correspondence does not give all the answers, it does provide many clues that historians can use to investigate her claims. I also hope that the publication of this article might persuade people who possess knowledge of Dr Ruddock’s research to come forward. For it is clear from her correspondence that many people must possess useful knowledge, ranging from her ex-students at the British Library to the “old and historic families in Italy” who gave her access to their private archives.’
As to why Alwyn Ruddock should have chosen to have all her research destroyed on her death, Dr Jones confesses that he has no clear answers. In her obituary in the Guardian newspaper, it was suggested that she destroyed the first draft of her book ‘because it did not meet her exacting standards.’ This does not explain, however, why she wanted everything destroyed – including her microfilms, her photographs and the transcripts of the documents she used.
‘What is clear,’ said Dr Jones, ‘is that she had a great sense of possession for her work and she felt this gave her the moral right to take her secrets to the grave. But even if all the documents she claimed to have found do come to light eventually, the mystery of why she sought to suppress her own basic research may never be resolved.’
Associated links
http://www.bristol.ac.uk/news/2007/5333.html
http://www.blackwell-synergy.com/toc/hisr/0/0
Joan of Arc relics exposed as a forgery
The relics of St Joan of Arc are not the remains of the fifteenth-century French heroine after all.European experts who have analysed the sacred scraps say the relics are a forgery, made from the remains of an Egyptian mummy.
Philippe Charlier, a forensic scientist obtained permission to study the relics -- cloth, a human rib and a cat femur -- from the French church last year. He says he was “astonished” by the results. “I’d never have thought that it could be from a mummy.”
The researchers used a range of techniques to investigate the remains, including mass, infrared and atomic-emission spectrometry, electron microscopy, pollen analysis and, unusually, the help of the leading ‘noses’ of the perfume industry: Sylvaine Delacourte from Guerlain, and Jean-Michel Duriez from Jean Patou.
A series of clues led to conclusion that the relics were of the mummy origin, reinforced by carbon-14 analysis dating the remains to between the third and sixth centuries BC. And the spectrometry profiles of the relics matched those from Egyptian mummies from the period, and not those of burnt bones.
Charlier points out that mummies were used in Europe during the Middle Ages in pharmaceutical remedies.
Contact:
Philippe Charlier (Raymond Poincare Hospital in Garches, Paris, France)
Tel: +33 1 40 10 76 89; E-mail: philippe.charlier@rpc.ap-hop-paris.fr
The relics of St Joan of Arc are not the remains of the fifteenth-century French heroine after all.European experts who have analysed the sacred scraps say the relics are a forgery, made from the remains of an Egyptian mummy.
Philippe Charlier, a forensic scientist obtained permission to study the relics -- cloth, a human rib and a cat femur -- from the French church last year. He says he was “astonished” by the results. “I’d never have thought that it could be from a mummy.”
The researchers used a range of techniques to investigate the remains, including mass, infrared and atomic-emission spectrometry, electron microscopy, pollen analysis and, unusually, the help of the leading ‘noses’ of the perfume industry: Sylvaine Delacourte from Guerlain, and Jean-Michel Duriez from Jean Patou.
A series of clues led to conclusion that the relics were of the mummy origin, reinforced by carbon-14 analysis dating the remains to between the third and sixth centuries BC. And the spectrometry profiles of the relics matched those from Egyptian mummies from the period, and not those of burnt bones.
Charlier points out that mummies were used in Europe during the Middle Ages in pharmaceutical remedies.
Contact:
Philippe Charlier (Raymond Poincare Hospital in Garches, Paris, France)
Tel: +33 1 40 10 76 89; E-mail: philippe.charlier@rpc.ap-hop-paris.fr
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