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Tuesday, September 6, 2011

World's Smallest Electric Motor Made from a Single Molecule


Chemists at Tufts University have developed the world's first single molecule electric motor, which may potentially create a new class of devices that could be used in applications ranging from medicine to engineering. The molecular motor was powered by electricity from a state of the art, low-temperature scanning tunneling microscope. This microscope sent an electrical current through the molecule, directing the molecule to rotate in one direction or another. The molecule had a sulfur base (yellow); when placed on a conductive slab of copper (orange), it became anchored to the surface. The sulfur-containing molecule had carbon and hydrogen atoms radiating off to form what looks like two arms (gray); these carbon chains were free to rotate around the central sulfur-copper bond. The researchers found that reducing the temperature of the molecule to five Kelvin (K), or about minus 450 degrees Fahrenheit (ºF), enabled them to precisely impact the direction and rotational speed of the molecular motor The Tufts team plans to submit this miniature electric motor to the Guinness World Records. The research was published online Sept. 4 in Nature Nanotechnology. (Credit: Heather L. Tierney, Colin J. Murphy, April D. Jewell, Ashleigh E. Baber, Erin V. Iski, Harout Y. Khodaverdian, Allister F. McGuire, Nikolai Klebanov and E. Charles H. Sykes.)

Science Daily  — The smallest electrical motor on the planet, at least according toGuinness World Records, is 200 nanometers. Granted, that's a pretty small motor -- after all, a single strand of human hair is 60,000 nanometers wide -- but that tiny mark is about to be shattered in a big way.
















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In research published online Sept. 4 in Nature Nanotechnology, the Tufts team reports an electric motor that measures a mere 1 nanometer across, groundbreaking work considering that the current world record is a 200 nanometer motor. A single strand of human hair is about 60,000 nanometers wide.
Chemists at Tufts University's School of Arts and Sciences have developed the world's first single molecule electric motor, a development that may potentially create a new class of devices that could be used in applications ranging from medicine to engineering.
According to E. Charles H. Sykes, Ph.D., associate professor of chemistry at Tufts and senior author on the paper, the team plans to submit the Tufts-built electric motor to Guinness World Records.
"There has been significant progress in the construction of molecular motors powered by light and by chemical reactions, but this is the first time that electrically-driven molecular motors have been demonstrated, despite a few theoretical proposals," says Sykes. "We have been able to show that you can provide electricity to a single molecule and get it to do something that is not just random."
Sykes and his colleagues were able to control a molecular motor with electricity by using a state of the art, low-temperature scanning tunneling microscope (LT-STM), one of about only 100 in the United States. The LT-STM uses electrons instead of light to "see" molecules.
The team used the metal tip on the microscope to provide an electrical charge to a butyl methyl sulfide molecule that had been placed on a conductive copper surface. This sulfur-containing molecule had carbon and hydrogen atoms radiating off to form what looked like two arms, with four carbons on one side and one on the other. These carbon chains were free to rotate around the sulfur-copper bond.
The team determined that by controlling the temperature of the molecule they could directly impact the rotation of the molecule. Temperatures around 5 Kelvin (K), or about minus 450 degrees Fahrenheit (ºF), proved to be the ideal to track the motor's motion. At this temperature, the Tufts researchers were able to track all of the rotations of the motor and analyze the data.
While there are foreseeable practical applications with this electric motor, breakthroughs would need to be made in the temperatures at which electric molecular motors operate. The motor spins much faster at higher temperatures, making it difficult to measure and control the rotation of the motor.
"Once we have a better grasp on the temperatures necessary to make these motors function, there could be real-world application in some sensing and medical devices which involve tiny pipes. Friction of the fluid against the pipe walls increases at these small scales, and covering the wall with motors could help drive fluids along," said Sykes. "Coupling molecular motion with electrical signals could also create miniature gears in nanoscale electrical circuits; these gears could be used in miniature delay lines, which are used in devices like cell phones."
The Changing Face of Chemistry
Students from the high school to the doctoral level played an integral role in the complex task of collecting and analyzing the movement of the tiny molecular motors.
"Involvement in this type of research can be an enlightening, and in some cases life changing, experience for students," said Sykes. "If we can get people interested in the sciences earlier, through projects like this, there is a greater chance we can impact the career they choose later in life."
As proof that gaining a scientific footing early can matter, one of the high school students involved in the research, Nikolai Klebanov, went on to enroll at Tufts; he is now a sophomore majoring in chemical engineering.
This work was supported by the National Science Foundation, the Beckman Foundation and the Research Corporation for Scientific Advancement.
Tufts University, located on three Massachusetts campuses in Boston, Medford/Somerville, and Grafton, and in Talloires, France, is recognized among the premier research universities in the United States. Tufts enjoys a global reputation for academic excellence and for the preparation of students as leaders in a wide range of professions. A growing number of innovative teaching and research initiatives span all campuses, and collaboration among the faculty and students in the undergraduate, graduate and professional programs across the university is widely encouraged.

Mystery of Disappearing Bird Digit Solved?


A genomic analysis shows that precursor cells pb that form index finger in five-fingered vertebrates can form the "thumb" (in orange) or first digit in three-digit bird wing (Credit: Courtesy Yale University)


Science Daily — What is the origin of digits in birds? The question has long puzzled evolutionary biologists. Using genomic analysis, researchers have now solved a key part of this mystery.














Yale scientists now have a good handle on how these developmental changes are orchestrated in the embryo. But there is still one outstanding debate on birds: Which digits are they? A thumb with index and middle fingers, or the index, middle and ring fingers?Evolution adds and subtracts, and nowhere is this math more evident than in vertebrates, which are programmed to have five digits on each limb. But many species do not. Snakes, of course, have no digits, and birds have three.In five-digit vertebrates, the thumb comes from the precursor stem cells labeled pa. While birds have a digit that looks like a thumb, pa precursor cells die off during development and never produce a digit in adults. As a result, scientists have wondered whether precursor cells in pb can make a thumb.
Yale scientists have completed a genomic analysis of birds that reveals the answer. It is a hands-down "yes" -- even though the first bird digit develops where the index finger on a five-finger vertebrae should be.
The results are published online Sept. 4 in the journal Nature. Authors are Zhe Wang, Rebecca L. Young, Huiling Xue, and Gunter P. Wagner from the Department of Ecology and 

Rock Rafts Could Be 'Cradle of Life'



Pumice from the Apex Chert, Australia c.3460m years old. (Credit: © Oxford University)


ScienceDaily — Floating rafts of volcanic pumice could have played a significant role in the origins of life on Earth, scientists from Oxford University and the University of Western Australia have suggested.










'Not only does pumice float as rafts but it has the highest surface-area-to-volume ratio of any type of rock, is exposed to a variety of conditions, and has the remarkable ability to adsorb metals, organics and phosphates as well as hosting organic catalysts, such as zeolites,' said Professor Martin Brasier of Oxford University's Department of Earth Sciences who led the work with David Wacey of the University of Western Australia. 'Taken together these properties suggest that it could have made an ideal 'floating laboratory' for the development of the earliest micro-organisms.'The researchers, writing in the September issue of the journalAstrobiology, argue that pumice has a unique set of properties which would have made it an ideal habitat for the earliest organisms that emerged on Earth over 3.5 billion years ago.The researchers believe that pumice's unique lifecycle -- in which it erupts from a volcano, then floats in rafts along the water's surface before entering the tidal zone, and then beaching for long periods close to shore -- would have presented many opportunities for life to develop.
'During its lifecycle pumice is potentially exposed to, among other things, lightning associated with volcanic eruptions, oily hydrocarbons and metals produced by hydrothermal vents, and ultraviolet light from the Sun as it floats on water,' said Professor Brasier. 'All these conditions have the potential to host, or even generate, the kind of chemical processes that we think created the first living cells.'
'We know that life was thriving between the pores of beach sand grains some 3,400 million years ago,' said David Wacey of the University of Western Australia, referring to the team's recent work in Nature Geoscience. 'What we are saying here is that certain kinds of beach might have provided a cradle for life.'
The team say that their hypothesis can be tested by examining the early fossil record for evidence of pumice rafts, and conducting laboratory experiments on pumice rocks to see if they can create new catalysts and compounds when exposed to cycles of heat and ultraviolet radiation

Chocolate linked to heart health, may reduce risk of heart disease



High levels of chocolate consumption might be associated with a one third reduction in the risk of developing heart disease, finds a study published on British Medical Journal last week.
Based on observational evidence, levels of chocolate consumption seem to be associated with a substantial reduction in the risk of cardiometabolic disorders.
The findings confirm results of existing studies that generally agree on a potential beneficial link between chocolate consumption and heart health. However, the authors stress that further studies are needed to test whether chocolate actually causes this reduction or if it can be explained by some other unmeasured (confounding) factor.
The findings will be presented at the European Society of Cardiology Congress in Paris at 10:10 hrs (Paris time) / 09:10 hrs (UK time) on Monday 29 August 2011.
The World Health Organisation predicts that by 2030, nearly 23.6 million people will die from heart disease. However, lifestyle and diet are key factors in preventing heart disease, says the paper.
A number of recent studies have shown that eating chocolate has a positive influence on human health due to its antioxidant and anti-inflammatory properties. This includes reducing blood pressure and improving insulin sensitivity (a stage in the development of diabetes).
However, the evidence about how eating chocolate affects your heart still remains unclear. So, Dr Oscar Franco and colleagues from the University of Cambridge carried out a large scale review of the existing evidence to evaluate the effects of eating chocolate on cardiovascular events like heart attack and stroke.
They analysed the results of seven studies, involving over 100,000 participants with and without existing heart disease. For each study, they compared the group with the highest chocolate consumption against the group with the lowest consumption. Differences in study design and quality were also taken into account to minimise bias.
Five studies reported a beneficial link between higher levels of chocolate consumption and the risk of cardiovascular events. They found that the “highest levels of chocolate consumption were associated with a 37% reduction in cardiovascular disease and a 29% reduction in stroke compared with lowest levels.” No significant reduction was found in relation to heart failure.
The studies did not differentiate between dark or milk chocolate and included consumption of chocolate bars, drinks, biscuits and desserts.
The authors say the findings need to be interpreted with caution, in particular because commercially available chocolate is very calorific (around 500 calories for every 100 grams) and eating too much of it could lead to weight gain, risk of diabetes and heart disease.
However, they conclude that given the health benefits of eating chocolate, initiatives to reduce the current fat and sugar content in most chocolate products should be explored.

Abstract From The Study

Objective: To evaluate the association of chocolate consumption with the risk of developing cardiometabolic disorders.
Design: Systematic review and meta-analysis of randomised controlled trials and observational studies.
Data sources: Medline, Embase, Cochrane Library, PubMed, CINAHL, IPA, Web of Science, Scopus, Pascal, reference lists of relevant studies to October 2010, and email contact with authors.
Study selection: Randomised trials and cohort, case-control, and cross sectional studies carried out in human adults, in which the association between chocolate consumption and the risk of outcomes related to cardiometabolic disorders were reported.
Data extraction: Data were extracted by two independent investigators, and a consensus was reached with the involvement of a third. The primary outcome was cardiometabolic disorders, including cardiovascular disease (coronary heart disease and stroke), diabetes, and metabolic syndrome. A meta-analysis assessed the risk of developing cardiometabolic disorders by comparing the highest and lowest level of chocolate consumption.
Results: From 4576 references seven studies met the inclusion criteria (including 114 009 participants). None of the studies was a randomised trial, six were cohort studies, and one a cross sectional study. Large variation was observed between these seven studies for measurement of chocolate consumption, methods, and outcomes evaluated. Five of the seven studies reported a beneficial association between higher levels of chocolate consumption and the risk of cardiometabolic disorders. The highest levels of chocolate consumption were associated with a 37% reduction in cardiovascular disease (relative risk 0.63 (95% confidence interval 0.44 to 0.90)) and a 29% reduction in stroke compared with the lowest levels.
Conclusions: Based on observational evidence, levels of chocolate consumption seem to be associated with a substantial reduction in the risk of cardiometabolic disorders. Further experimental studies are required to confirm a potentially beneficial effect of chocolate consumption.

Gene defect that predisposes people to leukemia discovered



“Those at risk because of family history may soon obtain tests to detect the genetic error before symptoms emerge.”
Caption: This is a close-up of a bone marrow slide photographed in 1992 by Daniel E. Sabath, University of Washington (UW) professor of laboratory medicine. Credit: Daniel E. Sabath
A new genetic defect that predisposes people to acute myeloid leukemia and myelodysplasia has been discovered. The mutations were found in the GATA2 gene. Among its several regulatory roles, the gene acts as a master control during the transition of primitive blood-forming cells into white blood cells.
The researchers started by studying four unrelated families who, over generations, have had several relatives with acute myeloid leukemia, a type of blood cancer. Their disease onset occurred from the teens to the early 40s. The course was rapid.
The findings will be reported Sept. 4 inNature Genetics. The results come from an international collaboration of scientists and the participation of families from Australia, Canada, and the United States.
In collaboration with Dr. Hamish Scott and Dr. Richard J. D’Andrea at the Centre for Cancer Biology, University of Australia, Adelaide, the U.S. portion of the study was conducted by Dr. Marshall Horwitz, University of Washington (UW) professor of pathology. Horwitz practices genetic medicine at UW Medical Center and the UW Center for Human Development and Disability, both in Seattle.
The genetic mutation was first discovered in a patient from central Washington. The research participant had been successfully treated for leukemia in 1992 through a bone marrow transplant at UW Medical Center. At that time, Horwitz decided to seek a possible genetic reason after learning his patient had several family members with myelodysplastic syndrome, myeloid leukemia, and intractable mycobacteria infections.
Myelodysplastic syndrome is a difficulty in producing certain kinds of blood cells. The problem originates in the bone marrow with a decline in the number and quality of blood-forming cells. Patients often have severe anemia and need frequent blood transfusions. The disease generally worsens due to bone marrow failure and low blood counts. About one- third of those with the syndrome soon develop acute myeloid leukemia, in which abnormal white cells build up in the bone marrow and interfere with normal blood production.
Horwitz’s Australian colleagues had described a family with a similarly inherited blood disorder. Eighteen years later, after rifling through many candidate genes, the researchers on both continents were relieved finally to have hit upon the mutated gene responsible for the leukemia that affect these families. They have gone on to identify abnormal GATA2 genes in more than 20 families and individuals.
Caption: This is a photograph of a bone marrow slide taken in 1992 by Daniel E. Sabath, University of Washington professor of laboratory medicine. Credit: Daniel E. Sabath
“It’s likely that this inherited error is more common than we had thought,” the researchers noted. In some families with a GATA2 mutation, the over-riding concern has been leukemia, while others suffer dangerous infections from bacteria, viruses and fungi because of a lack of white blood cells to fight off germs.
The lab of Dr. Dennis Hickstein, formerly of the UW School of Medicine and the Puget Sound Veterans Affairs Health System and now at the National Institute of Health, in collaboration with NIH colleague Dr. Steven Holland, associated the mutation with mycobacteria infections. Those results were reported in separate study appearing in the journal Blood.
Another paper appearing Sept. 4 in Nature Genetics from a London group found similar mutations of GATA2 in leukemia patients with lymphedema and, in some cases, deafnesss. By blocking the vessels that drain fluid from the body’s tissues, lympedema causes swelling of the arms or legs.
Ongoing work in Seattle and Adelaide has identified a congenital syndrome associated with developmental delay and a risk of myelodysplasia. This syndrome results from chromosomal loss of GATA2 and adjacent genes.
Comparable GATA2 mutations also have been found in people with the more common, non-inherited leukemias.
Scientists are trying to figure out why apparently similar gene mutations in GATA 2 cause such assorted health problems. Also perplexing is how hard it has been to find genetic errors underlying blood cancers, compared with other cancers.
Caption: Dr. Marshall S. Horwitz, professor of pathology at the University of Washington (UW) studies the genetics of blood cancers. Credit: University of Washington
“While several genes have been discovered and linked to solid, malignant tumors such as breast cancer in families susceptible to those types of cancer, so far very few inherited mutations have been uncovered for blood cancers,” Horwitz said.
Previously, other scientists linked mutations in two other genes — RUNX1 and CEBPA – to injerited forms of myelodysplastic syndrome and acute myeloid leukemia. These genes bind to DNA and control the copying of information encoded in this molecule.
Keeping this in mind, researchers looked for mutations in similar genes in families who did not have the RUNX1 and CEBPA mutations and who had no other explanations for their inherited blood cancer. In so doing, the researchers identified the GATA2 mutations. They also observed that these mutations relate to loss of function by making the gene unable to perform the molecular duties necessary to manufacture healthy white blood cells.
According to Horwitz, the GATA2 mutations in DNA occur adjacent to an amino acid mutated in some patients with terminal chronic myeloid leukemia. This proximity suggests a common pathway may be critical for several types of myeloid malignancies, he said.
People at risk because of their pedigree eventually may obtain tests to detect this genetic error before symptoms emerge. Learning that they have the gene mutation might help patients and their doctors decide on appropriate follow-up for early diagnosis and treatment of problems that might arise.
Additional knowledge about how the GATA2 gene and its mutations operate may foster the development of new therapeutic agents.
________________
A clinical trial under way in the United States may point to specific treatment recommendations for persons with a GATA2 genetic mutation.
The research for “Heritable GATA2 Mutations Associated with Familial Myelodysplastic Syndrome and Acute Myeloid Leukemia,” was supported by grants from the National Health and Medical Research Council of Australia, a Dora Lush Postgraduate Award, Leukaemia Foundation of Australia, the Cancer Council of South Australia, MedVet Pty Ltd., and the U.S. National Institutes of Health. 
The researchers extend their gratitude to the families and individuals who participated in this project.

Scientists announce human intestinal stem cell ‘breakthrough’ for regenerative medicine



“Human colon stem cells have been identified and grown in a lab-plate for the first time.”
This is the first time that it has been possible to grow single CoSCs in lab-plates and to derive human intestinal stem cell lines in defined conditions in a lab setting.
Human colon stem cells have been identified and grown in a lab-plate for the first time. This achievement, made by researchers of the Colorectal Cancer Lab at the Institute for Research in Biomedicine (IRB Barcelona) and published in Nature Medicine, is a crucial advance towards regenerative medicine.
Throughout life, stem cells of the colon regenerate the inner layer of our large intestine in a weekly basis. For decades scientists had evidences of the existence of these cells yet their identity remained elusive. Scientists led by the ICREA Professor and researcher at the Institute for Research in Biomedicine (IRB Barcelona) Eduard Batlle discovered the precise localization of the stem cells in the human colon and worked out a method that allows their isolation and in vitro expansion, that is their propagation in lab-plates.
Growing cells outside the body generally requires providing the cells in a lab-plate with the right mix of nutrients, growth factors and hormones. But in the same way that each of the more than 200 types of cells in our body differs from the others so too do optimal growing conditions in the lab. Consequently, human adult stem cell culture in labs has been a truly impossible mission until now.
Batlle’s team has also established the conditions for maintain living human colon stem cells (CoSCs) outside of the human body: “This is the first time that it has been possible to grow single CoSCs in lab-plates and to derive human intestinal stem cell lines in defined conditions in a lab setting,” explains the IRB Barcelona researcher Peter Jung, first author of the study together with Toshiro Sato, from the University Medical Center Utrecht in The Netherlands.
The development, published by Batlle’s research group in the prestigious journal Nature Medicine, arrives after more than 10 years of intense research focused on the characterization of the biology of the intestinal stem cells and its connection with cancer. The research has been made possible by close collaboration between Batlle’s team and the group led by Hans Clevers at the Hubretcht Institute and University Medical Center Utrecht in The Netherlands, and María A. Blasco at the Spanish National Cancer Research Centre in Madrid (Spain).
“For years, scientists all over the world have been trying to grow intestinal tissue in lab-plates; testing different conditions; using different nutritive media. But because the vast majority of cells in this tissue are in a differentiated state in which they do not proliferate, they survived only for a few days”, explains Jung.
“The aim of this study was to find a way to identify and select individual CoSCs and to grow them while maintaining their undifferentiated and proliferative state in lab conditions. Thus, we would be able to model how they grow —in number— and differentiate into normal intestinal epithelial cells in lab-plates”, continues Jung. The scientific community now has a defined ‘recipe’ for isolating CoSCs and deriving stable CoSCs lines, which have the capacity to grow undifferentiated for months. In fact, “now we can maintain stem cells in a plate up to 5 months or we can induce these cells to differentiate artificially, as they do inside our bodies”.
“This achievement opens up an exciting new area of research with the potential to bring about a huge breakthrough in regenerative medicine”, says Jung. Regenerative medicine — or the idea of repairing the body by developing new tissues and organs as the old ones wear out— involves growing new cells from patients into tissues and organs in a lab. However, the main element for making regenerative medicine a reality, namely adult stem cells, are just starting to be understood.
“Now that guidelines for growing and maintaining colon stem cells in the lab are in place, we have an ideal platform that could help the scientific community to determine the molecular bases of gastrointestinal cell proliferation and differentiation. It is also suspected that alterations in the biology of CoSCs are at origin of several diseases affecting the gastrointestinal tract, such as colorectal cancer or Crohn’s disease, an autoimmune and inflammatory disorder. Our discovery also paves the way to start exploring this exciting field,” finishes Jung.

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Ethiopia: What Equality Means to Me

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