source.txt

INSERT INTO `scidy` VALUES (2, '\'Ultra-small nanoprobes could be a leap forward in high-resolution human-machine interfaces\'', '\'July 3, 2019\'', '\'University of Surrey\'', '\'Machine enhanced humans -- or cyborgs as they are known in science fiction -- could be one step closer to becoming a reality, thanks to new research.\n\'', '\'\nResearchers have conquered the monumental task of manufacturing scalable nanoprobe arrays small enough to record the inner workings of human cardiac cells and primary neurons.\nThe ability to read electrical activities from cells is the foundation of many biomedical procedures, such as brain activity mapping and neural prosthetics. Developing new tools for intracellular electrophysiology (the electric current running within cells) that push the limits of what is physically possible (spatiotemporal resolution) while reducing invasiveness could provide a deeper understanding of electrogenic cells and their networks in tissues, as well as new directions for human-machine interfaces.\nIn a paper published by Nature Nanotechnology, scientists from Surrey\'s Advanced Technology Institute (ATI) and Harvard University detail how they produced an array of the ultra-small U-shaped nanowire field-effect transistor probes for intracellular recording. This incredibly small structure was used to record, with great clarity, the inner activity of primary neurons and other electrogenic cells, and the device has the capacity for multi-channel recordings.\nDr Yunlong Zhao from the ATI at the University of Surrey said: \"If our medical professionals are to continue to understand our physical condition better and help us live longer, it is important that we continue to push the boundaries of modern science in order to give them the best possible tools to do their jobs. For this to be possible, an intersection between humans and machines is inevitable.\n\"Our ultra-small, flexible, nanowire probes could be a very powerful tool as they can measure intracellular signals with amplitudes comparable with those measured with patch clamp techniques; with the advantage of the device being scalable, it causes less discomfort and no fatal damage to the cell (cytosol dilation). Through this work, we found clear evidence for how both size and curvature affect device internalisation and intracellular recording signal.\"\nProfessor Charles Lieber from the Department of Chemistry and Chemical Biology at Harvard University said: \"This work represents a major step towards tackling the general problem of integrating \'synthesised\' nanoscale building blocks into chip and wafer scale arrays, and thereby allowing us to address the long-standing challenge of scalable intracellular recording.\n\"The beauty of science to many, ourselves included, is having such challenges to drive hypotheses and future work. In the longer term, we see these probe developments adding to our capabilities that ultimately drive advanced high-resolution brain-machine interfaces and perhaps eventually bringing cyborgs to reality.\"\nProfessor Ravi Silva, Director of the ATI at the University of Surrey, said: \"This incredibly exciting and ambitious piece of work illustrates the value of academic collaboration. Along with the possibility of upgrading the tools we use to monitor cells, this work has laid the foundations for machine and human interfaces that could improve lives across the world.\"\nDr Yunlong Zhao and his team are currently working on novel energy storage devices, electrochemical probing, bioelectronic devices, sensors and 3D soft electronic systems. Undergraduate, graduate and postdoc students with backgrounds in energy storage, electrochemistry, nanofabrication, bioelectronics, tissue engineering are very welcome to contact Dr Zhao to explore the opportunities further.\n\'', '\'Materials provided by University of Surrey. Note: Content may be edited for style and length.\'', '\'\nYunlong Zhao, Siheng Sean You, Anqi Zhang, Jae-Hyun Lee, Jinlin Huang, Charles M. Lieber. Scalable ultrasmall three-dimensional nanowire transistor probes for intracellular recording. Nature Nanotechnology, 2019; DOI: 10.1038/s41565-019-0478-y\n\n\'', '\'https://www.sciencedaily.com/releases/2019/07/190703121358.htm\n\'');
INSERT INTO `scidy` VALUES (5, '\'Using artificial intelligence to better predict severe weather\'', '\'July 2, 2019\'', '\'Penn State\'', '\'When forecasting weather, meteorologists use a number of models and data sources to track shapes and movements of clouds that could indicate severe storms. However, with increasingly expanding weather data sets and looming deadlines, it is nearly impossible for them to monitor all storm formations -- especially smaller-scale ones -- in real time.\n\'', '\'\nNow, there is a computer model that can help forecasters recognize potential severe storms more quickly and accurately, thanks to a team of researchers at Penn State, AccuWeather, Inc., and the University of Almería in Spain. They have developed a framework based on machine learning linear classifiers -- a kind of artificial intelligence -- that detects rotational movements in clouds from satellite images that might have otherwise gone unnoticed. This AI solution ran on the Bridges supercomputer at the Pittsburgh Supercomputing Center.\nSteve Wistar, senior forensic meteorologist at AccuWeather, said that having this tool to point his eye toward potentially threatening formations could help him to make a better forecast.\n\"The very best forecasting incorporates as much data as possible,\" he said. \"There\'s so much to take in, as the atmosphere is infinitely complex. By using the models and the data we have [in front of us], we\'re taking a snapshot of the most complete look of the atmosphere.\"\nIn their study, the researchers worked with Wistar and other AccuWeather meteorologists to analyze more than 50,000 historical U.S. weather satellite images. In them, experts identified and labeled the shape and motion of \"comma-shaped\" clouds. These cloud patterns are strongly associated with cyclone formations, which can lead to severe weather events including hail, thunderstorms, high winds and blizzards.\nThen, using computer vision and machine learning techniques, the researchers taught computers to automatically recognize and detect comma-shaped clouds in satellite images. The computers can then assist experts by pointing out in real time where, in an ocean of data, could they focus their attention in order to detect the onset of severe weather.\n\"Because the comma-shaped cloud is a visual indicator of severe weather events, our scheme can help meteorologists forecast such events,\" said Rachel Zheng, a doctoral student in the College of Information Sciences and Technology at Penn State and the main researcher on the project.\nThe researchers found that their method can effectively detect comma-shaped clouds with 99 percent accuracy, at an average of 40 seconds per prediction. It was also able to predict 64 percent of severe weather events, outperforming other existing severe-weather detection methods.\n\"Our method can capture most human-labeled, comma-shaped clouds,\" said Zheng. \"Moreover, our method can detect some comma-shaped clouds before they are fully formed, and our detections are sometimes earlier than human eye recognition.\"\n\"The calling of our business is to save lives and protect property,\" added Wistar. \"The more advanced notice to people that would be affected by a storm, the better we\'re providing that service. We\'re trying to get the best information out as early as possible.\"\nThis project enhances earlier work between AccuWeather and a College of IST research group led by professor James Wang, who is the dissertation adviser of Zheng.\n\"We recognized when our collaboration began [with AccuWeather in 2010] that a significant challenge facing meteorologists and climatologists was in making sense of the vast and continually increasing amount of data generated by Earth observation satellites, radars and sensor networks,\" said Wang. \"It is essential to have computerized systems analyze and learn from the data so we can provide timely and proper interpretation of the data in time-sensitive applications such as severe-weather forecasting.\"\nHe added, \"This research is an early attempt to show feasibility of artificial intelligence-based interpretation of weather-related visual information to the research community. More research to integrate this approach with existing numerical weather-prediction models and other simulation models will likely make the weather forecast more accurate and useful to people.\"\nConcluded Wistar, \"The benefit [of this research] is calling the attention of a very busy forecaster to something that may have otherwise been overlooked.\"\n\'', '\'Materials provided by Penn State. Original written by Jessica Hallman. Note: Content may be edited for style and length.\'', '\'\nXinye Zheng, Jianbo Ye, Yukun Chen, Steve Wistar, Jia Li, Jose A. Piedra Fernandez, Michael A. Steinberg, James Z. Wang. Detecting Comma-Shaped Clouds for Severe Weather Forecasting Using Shape and Motion. IEEE Transactions on Geoscience and Remote Sensing, 2019; 57 (6): 3788 DOI: 10.1109/TGRS.2018.2887206\n\n\'', '\'https://www.sciencedaily.com/releases/2019/07/190702160115.htm\n\'');
INSERT INTO `scidy` VALUES (18, '\'Tiny motor can \'walk\' to carry out tasks\'', '\'July 2, 2019\'', '\'Massachusetts Institute of Technology\'', '\'Researchers have assembled microrobots from a small set of standardized components, as a step toward self-replicating systems.\n\'', '\'\nGershenfeld and his students have been making steady progress in that direction ever since. Their latest achievement, presented this week at an international robotics conference, consists of a set of five tiny fundamental parts that can be assembled into a wide variety of functional devices, including a tiny \"walking\" motor that can move back and forth across a surface or turn the gears of a machine.\nPreviously, Gershenfeld and his students showed that structures assembled from many small, identical subunits can have numerous mechanical properties. Next, they demonstrated that a combination of rigid and flexible part types can be used to create morphing airplane wings, a longstanding goal in aerospace engineering. Their latest work adds components for movement and logic, and will be presented at the International Conference on Manipulation, Automation and Robotics at Small Scales (MARSS) in Helsinki, Finland, in a paper by Gershenfeld and MIT graduate student Will Langford.\nTheir work offers an alternative to today\'s approaches to constructing robots, which largely fall into one of two types: custom machines that work well but are relatively expensive and inflexible, and reconfigurable ones that sacrifice performance for versatility. In the new approach, Langford came up with a set of five millimeter-scale components, all of which can be attached to each other by a standard connector. These parts include the previous rigid and flexible types, along with electromagnetic parts, a coil, and a magnet. In the future, the team plans to make these out of still smaller basic part types.\nUsing this simple kit of tiny parts, Langford assembled them into a novel kind of motor that moves an appendage in discrete mechanical steps, which can be used to turn a gear wheel, and a mobile form of the motor that turns those steps into locomotion, allowing it to \"walk\" across a surface in a way that is reminiscent of the molecular motors that move muscles. These parts could also be assembled into hands for gripping, or legs for walking, as needed for a particular task, and then later reassembled as those needs change. Gershenfeld refers to them as \"digital materials,\" discrete parts that can be reversibly joined, forming a kind of functional micro-LEGO.\nThe new system is a significant step toward creating a standardized kit of parts that could be used to assemble robots with specific capabilities adapted to a particular task or set of tasks. Such purpose-built robots could then be disassembled and reassembled as needed in a variety of forms, without the need to design and manufacture new robots from scratch for each application.\nLangford\'s initial motor has an ant-like ability to lift seven times its own weight. But if greater forces are required, many of these parts can be added to provide more oomph. Or if the robot needs to move in more complex ways, these parts could be distributed throughout the structure. The size of the building blocks can be chosen to match their application; the team has made nanometer-sized parts to make nanorobots, and meter-sized parts to make megarobots. Previously, specialized techniques were needed at each of these length scale extremes.\n\"One emerging application is to make tiny robots that can work in confined spaces,\" Gershenfeld says. Some of the devices assembled in this project, for example, are smaller than a penny yet can carry out useful tasks.\nTo build in the \"brains,\" Langford has added part types that contain millimeter-sized integrated circuits, along with a few other part types to take care of connecting electrical signals in three dimensions.\nThe simplicity and regularity of these structures makes it relatively easy for their assembly to be automated. To do that, Langford has developed a novel machine that\'s like a cross between a 3-D printer and the pick-and-place machines that manufacture electronic circuits, but unlike either of those, this one can produce complete robotic systems directly from digital designs. Gershenfeld says this machine is a first step toward to the project\'s ultimate goal of \"making an assembler that can assemble itself out of the parts that it\'s assembling.\"\n\'', '\'Materials provided by Massachusetts Institute of Technology. Original written by David L. Chandler. Note: Content may be edited for style and length.\'', 'NULL', '\'https://www.sciencedaily.com/releases/2019/07/190702152751.htm\n\'');
INSERT INTO `scidy` VALUES (24, '\'Tiny motor can \'walk\' to carry out tasks\'', '\'July 2, 2019\'', '\'Massachusetts Institute of Technology\'', '\'Researchers have assembled microrobots from a small set of standardized components, as a step toward self-replicating systems.\n\'', '\'\nGershenfeld and his students have been making steady progress in that direction ever since. Their latest achievement, presented this week at an international robotics conference, consists of a set of five tiny fundamental parts that can be assembled into a wide variety of functional devices, including a tiny \"walking\" motor that can move back and forth across a surface or turn the gears of a machine.\nPreviously, Gershenfeld and his students showed that structures assembled from many small, identical subunits can have numerous mechanical properties. Next, they demonstrated that a combination of rigid and flexible part types can be used to create morphing airplane wings, a longstanding goal in aerospace engineering. Their latest work adds components for movement and logic, and will be presented at the International Conference on Manipulation, Automation and Robotics at Small Scales (MARSS) in Helsinki, Finland, in a paper by Gershenfeld and MIT graduate student Will Langford.\nTheir work offers an alternative to today\'s approaches to constructing robots, which largely fall into one of two types: custom machines that work well but are relatively expensive and inflexible, and reconfigurable ones that sacrifice performance for versatility. In the new approach, Langford came up with a set of five millimeter-scale components, all of which can be attached to each other by a standard connector. These parts include the previous rigid and flexible types, along with electromagnetic parts, a coil, and a magnet. In the future, the team plans to make these out of still smaller basic part types.\nUsing this simple kit of tiny parts, Langford assembled them into a novel kind of motor that moves an appendage in discrete mechanical steps, which can be used to turn a gear wheel, and a mobile form of the motor that turns those steps into locomotion, allowing it to \"walk\" across a surface in a way that is reminiscent of the molecular motors that move muscles. These parts could also be assembled into hands for gripping, or legs for walking, as needed for a particular task, and then later reassembled as those needs change. Gershenfeld refers to them as \"digital materials,\" discrete parts that can be reversibly joined, forming a kind of functional micro-LEGO.\nThe new system is a significant step toward creating a standardized kit of parts that could be used to assemble robots with specific capabilities adapted to a particular task or set of tasks. Such purpose-built robots could then be disassembled and reassembled as needed in a variety of forms, without the need to design and manufacture new robots from scratch for each application.\nLangford\'s initial motor has an ant-like ability to lift seven times its own weight. But if greater forces are required, many of these parts can be added to provide more oomph. Or if the robot needs to move in more complex ways, these parts could be distributed throughout the structure. The size of the building blocks can be chosen to match their application; the team has made nanometer-sized parts to make nanorobots, and meter-sized parts to make megarobots. Previously, specialized techniques were needed at each of these length scale extremes.\n\"One emerging application is to make tiny robots that can work in confined spaces,\" Gershenfeld says. Some of the devices assembled in this project, for example, are smaller than a penny yet can carry out useful tasks.\nTo build in the \"brains,\" Langford has added part types that contain millimeter-sized integrated circuits, along with a few other part types to take care of connecting electrical signals in three dimensions.\nThe simplicity and regularity of these structures makes it relatively easy for their assembly to be automated. To do that, Langford has developed a novel machine that\'s like a cross between a 3-D printer and the pick-and-place machines that manufacture electronic circuits, but unlike either of those, this one can produce complete robotic systems directly from digital designs. Gershenfeld says this machine is a first step toward to the project\'s ultimate goal of \"making an assembler that can assemble itself out of the parts that it\'s assembling.\"\n\'', '\'Materials provided by Massachusetts Institute of Technology. Original written by David L. Chandler. Note: Content may be edited for style and length.\'', 'NULL', '\'https://www.sciencedaily.com/releases/2019/07/190702152751.htm\n\'');
INSERT INTO `scidy` VALUES (25, '\'HIV eliminated from the genomes of living animals\'', '\'July 2, 2019\'', '\'Temple University Health System\'', '\'Researchers have for the first time eliminated replication-competent HIV-1 DNA -- the virus responsible for AIDS -- from the genomes of living animals. The study marks a critical step toward the development of a possible cure for human HIV infection.\n\'', '\'\n\"Our study shows that treatment to suppress HIV replication and gene editing therapy, when given sequentially, can eliminate HIV from cells and organs of infected animals,\" said Kamel Khalili, PhD, Laura H. Carnell Professor and Chair of the Department of Neuroscience, Director of the Center for Neurovirology, and Director of the Comprehensive NeuroAIDS Center at the Lewis Katz School of Medicine at Temple University (LKSOM). Dr. Khalili and Howard Gendelman, MD, Margaret R. Larson Professor of Infectious Diseases and Internal Medicine, Chair of the Department of Pharmacology and Experimental Neuroscience and Director of the Center for Neurodegenerative Diseases at UNMC, were senior investigators on the new study.\n\"This achievement could not have been possible without an extraordinary team effort that included virologists, immunologists, molecular biologists, pharmacologists, and pharmaceutical experts,\" Dr. Gendelman said. \"Only by pooling our resources together were we able to make this groundbreaking discovery.\"\nCurrent HIV treatment focuses on the use of antiretroviral therapy (ART). ART suppresses HIV replication but does not eliminate the virus from the body. Therefore, ART is not a cure for HIV, and it requires life-long use. If it is stopped, HIV rebounds, renewing replication and fueling the development of AIDS. HIV rebound is directly attributed to the ability of the virus to integrate its DNA sequence into the genomes of cells of the immune system, where it lies dormant and beyond the reach of antiretroviral drugs.\nIn previous work, Dr. Khalili\'s team used CRISPR-Cas9 technology to develop a novel gene editing and gene therapy delivery system aimed at removing HIV DNA from genomes harboring the virus. In rats and mice, they showed that the gene editing system could effectively excise large fragments of HIV DNA from infected cells, significantly impacting viral gene expression. Similar to ART, however, gene editing cannot completely eliminate HIV on its own.\nFor the new study, Dr. Khalili and colleagues combined their gene editing system with a recently developed therapeutic strategy known as long-acting slow-effective release (LASER) ART. LASER ART was co-developed by Dr. Gendelman and Benson Edagwa, PhD, Assistant Professor of Pharmacology at UNMC.\nLASER ART targets viral sanctuaries and maintains HIV replication at low levels for extended periods of time, reducing the frequency of ART administration. The long-lasting medications were made possible by pharmacological changes in the chemical structure of the antiretroviral drugs. The modified drug was packaged into nanocrystals, which readily distribute to tissues where HIV is likely to be lying dormant. From there, the nanocrystals, stored within cells for weeks, slowly release the drug.\nAccording to Dr. Khalili, \"We wanted to see whether LASER ART could suppress HIV replication long enough for CRISPR-Cas9 to completely rid cells of viral DNA.\"\nTo test their idea, the researchers used mice engineered to produce human T cells susceptible to HIV infection, permitting long-term viral infection and ART-induced latency. Once infection was established, mice were treated with LASER ART and subsequently with CRISPR-Cas9. At the end of the treatment period, mice were examined for viral load. Analyses revealed complete elimination of HIV DNA in about one-third of HIV-infected mice.\n\"The big message of this work is that it takes both CRISPR-Cas9 and virus suppression through a method such as LASER ART, administered together, to produce a cure for HIV infection,\" Dr. Khalili said. \"We now have a clear path to move ahead to trials in non-human primates and possibly clinical trials in human patients within the year.\"\n\'', '\'Materials provided by Temple University Health System. Note: Content may be edited for style and length.\'', '\'\nPrasanta K. Dash, Rafal Kaminski, Ramona Bella, Hang Su, Saumi Mathews, Taha M. Ahooyi, Chen Chen, Pietro Mancuso, Rahsan Sariyer, Pasquale Ferrante, Martina Donadoni, Jake A. Robinson, Brady Sillman, Zhiyi Lin, James R. Hilaire, Mary Banoub, Monalisha Elango, Nagsen Gautam, R. Lee Mosley, Larisa Y. Poluektova, JoEllyn McMillan, Aditya N. Bade, Santhi Gorantla, Ilker K. Sariyer, Tricia H. Burdo, Won-Bin Young, Shohreh Amini, Jennifer Gordon, Jeffrey M. Jacobson, Benson Edagwa, Kamel Khalili, Howard E. Gendelman. Sequential LASER ART and CRISPR Treatments Eliminate HIV-1 in a Subset of Infected Humanized Mice. Nature Communications, 2019; 10 (1) DOI: 10.1038/s41467-019-10366-y\n\n\'', '\'https://www.sciencedaily.com/releases/2019/07/190702112844.htm\n\'');
INSERT INTO `scidy` VALUES (27, '\'Neural nets to simulate molecular motion cast\'', '\'July 2, 2019\'', '\'DOE/Los Alamos National Laboratory\'', '\'New work is showing that artificial neural nets can be trained to encode quantum mechanical laws to describe the motions of molecules, supercharging simulations potentially across a broad range of fields.\n\'', '\'\n\"This means we can now model materials and molecular dynamics billions of times faster compared to conventional quantum methods, while retaining the same level of accuracy,\" said Justin Smith, Los Alamos physicist and Metropolis Fellow in the laboratory\'s Theoretical Division. Understanding how molecules move is critical to tapping their potential value for drug development, protein simulations and reactive chemistry, for example, and both quantum mechanics and experimental (empirical) methods feed into the simulations.\nThe new technique, called the ANI-1ccx potential, promises to advance the capabilities of researchers in many fields and improve the accuracy of machine learning-based potentials in future studies of metal alloys and detonation physics.\nQuantum mechanical (QM) algorithms, used on classical computers, can accurately describe the mechanical motions of a compound in its operational environment. But QM scales very poorly with varying molecular sizes, severely limiting the scope of possible simulations. Even a slight increase in molecular size within a simulation can dramatically increase the computational burden. So practitioners often resort to using empirical information, which describes the motion of atoms in terms of classical physics and Newton\'s Laws, enabling simulations that scale to billions of atoms or millions of chemical compounds.\nTraditionally, empirical potentials have had to strike a tradeoff between accuracy and transferability. When the many parameters of the potential are finely tuned for one compound, the accuracy decreases on other compounds.\nInstead, the Los Alamos team, with the University of North Carolina at Chapel Hill and University of Florida, has developed a machine learning approach called transfer learning that lets them build empirical potentials by learning from data collected about millions of other compounds. The new approach with the machine learning empirical potential can be applied to new molecules in milliseconds, enabling research into a far greater number of compounds over much longer timescales.\nFunding\nThe Los Alamos authors acknowledge support of the U.S. Department of Energy (DOE) through the LANL LDRD Program. This work was performed, in part, at the Center for Integrated Nanotechnologies, an Office of Science User Facility operated for the U.S. DOE Office of Science. They also acknowledge the LANL Institutional Computing (IC) program and LANL ACL data team for providing computational resources. This research in part was done using resources provided by the Open Science Grid which is supported by the National Science Foundation award 1148698, and the U.S. DOE Office of Science.\n\'', '\'Materials provided by DOE/Los Alamos National Laboratory. Note: Content may be edited for style and length.\'', '\'\nJustin S. Smith, Benjamin T. Nebgen, Roman Zubatyuk, Nicholas Lubbers, Christian Devereux, Kipton Barros, Sergei Tretiak, Olexandr Isayev, Adrian E. Roitberg. Approaching coupled cluster accuracy with a general-purpose neural network potential through transfer learning. Nature Communications, 2019; 10 (1) DOI: 10.1038/s41467-019-10827-4\n\n\'', '\'https://www.sciencedaily.com/releases/2019/07/190702184603.htm\n\'');
INSERT INTO `scidy` VALUES (28, '\'A short bout of exercise enhances brain function\'', '\'July 2, 2019\'', '\'Oregon Health & Science University\'', '\'Neuroscientists, working with mice, have discovered that a short burst of exercise directly boosts the function of a gene that increases connections between neurons in the hippocampus, the region of the brain associated with learning and memory.\n\'', '\'\nNeuroscientists at OHSU in Portland, Oregon, working with mice, have discovered that a short burst of exercise directly boosts the function of a gene that increases connections between neurons in the hippocampus, the region of the brain associated with learning and memory.\nThe research is published online in the journal eLife.\n\"Exercise is cheap, and you don\'t necessarily need a fancy gym membership or have to run 10 miles a day,\" said co-senior author Gary Westbrook, M.D., senior scientist at the OHSU Vollum Institute and Dixon Professor of Neurology in the OHSU School of Medicine.\nPrevious research in animals and in people shows that regular exercise promotes general brain health. However, it\'s hard to untangle the overall benefits of exercise to the heart, liver and muscles from the specific effect on the brain. For example, a healthy heart oxygenates the whole body, including the brain.\n\"Previous studies of exercise almost all focus on sustained exercise,\" Westbrook said. \"As neuroscientists, it\'s not that we don\'t care about the benefits on the heart and muscles but we wanted to know the brain-specific benefit of exercise.\"\nSo the scientists designed a study in mice that specifically measured the brain\'s response to single bouts of exercise in otherwise sedentary mice that were placed for short periods on running wheels. The mice ran a few kilometers in two hours.\nThe study found that short-term bursts of exercise -- the human equivalent of a weekly game of pickup basketball, or 4,000 steps -- promoted an increase in synapses in the hippocampus. Scientists made the key discovery by analyzing genes that were increased in single neurons activated during exercise.\nOne particular gene stood out: Mtss1L. This gene had been largely ignored in prior studies in the brain.\n\"That was the most exciting thing,\" said co-lead author Christina Chatzi, Ph.D.\nThe Mtss1L gene encodes a protein that causes bending of the cell membrane. Researchers discovered that when this gene is activated by short bursts of exercise, it promotes small growths on neurons known as dendritic spines -- the site at which synapses form.\nIn effect, the study showed that an acute burst of exercise is enough to prime the brain for learning.\nIn the next stage of research, scientists plan to pair acute bouts of exercise with learning tasks to better understand the impact on learning and memory.\n\'', '\'Materials provided by Oregon Health & Science University. Original written by Erik Robinson. Note: Content may be edited for style and length.\'', '\'\nChristina Chatzi, Gina Zhang, Wiiliam D Hendricks, Yang Chen, Eric Schnell, Richard H Goodman, Gary L Westbrook. Exercise-induced enhancement of synaptic function triggered by the inverse BAR protein, Mtss1L. eLife, 2019; 8 DOI: 10.7554/eLife.45920\n\n\'', '\'https://www.sciencedaily.com/releases/2019/07/190702184555.htm\n\'');
INSERT INTO `scidy` VALUES (30, '\'Tiny motor can \'walk\' to carry out tasks\'', '\'July 2, 2019\'', '\'Massachusetts Institute of Technology\'', '\'Researchers have assembled microrobots from a small set of standardized components, as a step toward self-replicating systems.\n\'', '\'\nGershenfeld and his students have been making steady progress in that direction ever since. Their latest achievement, presented this week at an international robotics conference, consists of a set of five tiny fundamental parts that can be assembled into a wide variety of functional devices, including a tiny \"walking\" motor that can move back and forth across a surface or turn the gears of a machine.\nPreviously, Gershenfeld and his students showed that structures assembled from many small, identical subunits can have numerous mechanical properties. Next, they demonstrated that a combination of rigid and flexible part types can be used to create morphing airplane wings, a longstanding goal in aerospace engineering. Their latest work adds components for movement and logic, and will be presented at the International Conference on Manipulation, Automation and Robotics at Small Scales (MARSS) in Helsinki, Finland, in a paper by Gershenfeld and MIT graduate student Will Langford.\nTheir work offers an alternative to today\'s approaches to constructing robots, which largely fall into one of two types: custom machines that work well but are relatively expensive and inflexible, and reconfigurable ones that sacrifice performance for versatility. In the new approach, Langford came up with a set of five millimeter-scale components, all of which can be attached to each other by a standard connector. These parts include the previous rigid and flexible types, along with electromagnetic parts, a coil, and a magnet. In the future, the team plans to make these out of still smaller basic part types.\nUsing this simple kit of tiny parts, Langford assembled them into a novel kind of motor that moves an appendage in discrete mechanical steps, which can be used to turn a gear wheel, and a mobile form of the motor that turns those steps into locomotion, allowing it to \"walk\" across a surface in a way that is reminiscent of the molecular motors that move muscles. These parts could also be assembled into hands for gripping, or legs for walking, as needed for a particular task, and then later reassembled as those needs change. Gershenfeld refers to them as \"digital materials,\" discrete parts that can be reversibly joined, forming a kind of functional micro-LEGO.\nThe new system is a significant step toward creating a standardized kit of parts that could be used to assemble robots with specific capabilities adapted to a particular task or set of tasks. Such purpose-built robots could then be disassembled and reassembled as needed in a variety of forms, without the need to design and manufacture new robots from scratch for each application.\nLangford\'s initial motor has an ant-like ability to lift seven times its own weight. But if greater forces are required, many of these parts can be added to provide more oomph. Or if the robot needs to move in more complex ways, these parts could be distributed throughout the structure. The size of the building blocks can be chosen to match their application; the team has made nanometer-sized parts to make nanorobots, and meter-sized parts to make megarobots. Previously, specialized techniques were needed at each of these length scale extremes.\n\"One emerging application is to make tiny robots that can work in confined spaces,\" Gershenfeld says. Some of the devices assembled in this project, for example, are smaller than a penny yet can carry out useful tasks.\nTo build in the \"brains,\" Langford has added part types that contain millimeter-sized integrated circuits, along with a few other part types to take care of connecting electrical signals in three dimensions.\nThe simplicity and regularity of these structures makes it relatively easy for their assembly to be automated. To do that, Langford has developed a novel machine that\'s like a cross between a 3-D printer and the pick-and-place machines that manufacture electronic circuits, but unlike either of those, this one can produce complete robotic systems directly from digital designs. Gershenfeld says this machine is a first step toward to the project\'s ultimate goal of \"making an assembler that can assemble itself out of the parts that it\'s assembling.\"\n\'', '\'Materials provided by Massachusetts Institute of Technology. Original written by David L. Chandler. Note: Content may be edited for style and length.\'', 'NULL', '\'https://www.sciencedaily.com/releases/2019/07/190702152751.htm\n\'');
INSERT INTO `scidy` VALUES (31, '\'HIV eliminated from the genomes of living animals\'', '\'July 2, 2019\'', '\'Temple University Health System\'', '\'Researchers have for the first time eliminated replication-competent HIV-1 DNA -- the virus responsible for AIDS -- from the genomes of living animals. The study marks a critical step toward the development of a possible cure for human HIV infection.\n\'', '\'\n\"Our study shows that treatment to suppress HIV replication and gene editing therapy, when given sequentially, can eliminate HIV from cells and organs of infected animals,\" said Kamel Khalili, PhD, Laura H. Carnell Professor and Chair of the Department of Neuroscience, Director of the Center for Neurovirology, and Director of the Comprehensive NeuroAIDS Center at the Lewis Katz School of Medicine at Temple University (LKSOM). Dr. Khalili and Howard Gendelman, MD, Margaret R. Larson Professor of Infectious Diseases and Internal Medicine, Chair of the Department of Pharmacology and Experimental Neuroscience and Director of the Center for Neurodegenerative Diseases at UNMC, were senior investigators on the new study.\n\"This achievement could not have been possible without an extraordinary team effort that included virologists, immunologists, molecular biologists, pharmacologists, and pharmaceutical experts,\" Dr. Gendelman said. \"Only by pooling our resources together were we able to make this groundbreaking discovery.\"\nCurrent HIV treatment focuses on the use of antiretroviral therapy (ART). ART suppresses HIV replication but does not eliminate the virus from the body. Therefore, ART is not a cure for HIV, and it requires life-long use. If it is stopped, HIV rebounds, renewing replication and fueling the development of AIDS. HIV rebound is directly attributed to the ability of the virus to integrate its DNA sequence into the genomes of cells of the immune system, where it lies dormant and beyond the reach of antiretroviral drugs.\nIn previous work, Dr. Khalili\'s team used CRISPR-Cas9 technology to develop a novel gene editing and gene therapy delivery system aimed at removing HIV DNA from genomes harboring the virus. In rats and mice, they showed that the gene editing system could effectively excise large fragments of HIV DNA from infected cells, significantly impacting viral gene expression. Similar to ART, however, gene editing cannot completely eliminate HIV on its own.\nFor the new study, Dr. Khalili and colleagues combined their gene editing system with a recently developed therapeutic strategy known as long-acting slow-effective release (LASER) ART. LASER ART was co-developed by Dr. Gendelman and Benson Edagwa, PhD, Assistant Professor of Pharmacology at UNMC.\nLASER ART targets viral sanctuaries and maintains HIV replication at low levels for extended periods of time, reducing the frequency of ART administration. The long-lasting medications were made possible by pharmacological changes in the chemical structure of the antiretroviral drugs. The modified drug was packaged into nanocrystals, which readily distribute to tissues where HIV is likely to be lying dormant. From there, the nanocrystals, stored within cells for weeks, slowly release the drug.\nAccording to Dr. Khalili, \"We wanted to see whether LASER ART could suppress HIV replication long enough for CRISPR-Cas9 to completely rid cells of viral DNA.\"\nTo test their idea, the researchers used mice engineered to produce human T cells susceptible to HIV infection, permitting long-term viral infection and ART-induced latency. Once infection was established, mice were treated with LASER ART and subsequently with CRISPR-Cas9. At the end of the treatment period, mice were examined for viral load. Analyses revealed complete elimination of HIV DNA in about one-third of HIV-infected mice.\n\"The big message of this work is that it takes both CRISPR-Cas9 and virus suppression through a method such as LASER ART, administered together, to produce a cure for HIV infection,\" Dr. Khalili said. \"We now have a clear path to move ahead to trials in non-human primates and possibly clinical trials in human patients within the year.\"\n\'', '\'Materials provided by Temple University Health System. Note: Content may be edited for style and length.\'', '\'\nPrasanta K. Dash, Rafal Kaminski, Ramona Bella, Hang Su, Saumi Mathews, Taha M. Ahooyi, Chen Chen, Pietro Mancuso, Rahsan Sariyer, Pasquale Ferrante, Martina Donadoni, Jake A. Robinson, Brady Sillman, Zhiyi Lin, James R. Hilaire, Mary Banoub, Monalisha Elango, Nagsen Gautam, R. Lee Mosley, Larisa Y. Poluektova, JoEllyn McMillan, Aditya N. Bade, Santhi Gorantla, Ilker K. Sariyer, Tricia H. Burdo, Won-Bin Young, Shohreh Amini, Jennifer Gordon, Jeffrey M. Jacobson, Benson Edagwa, Kamel Khalili, Howard E. Gendelman. Sequential LASER ART and CRISPR Treatments Eliminate HIV-1 in a Subset of Infected Humanized Mice. Nature Communications, 2019; 10 (1) DOI: 10.1038/s41467-019-10366-y\n\n\'', '\'https://www.sciencedaily.com/releases/2019/07/190702112844.htm\n\'');
INSERT INTO `scidy` VALUES (32, '\'The neuroscience of autism: New clues for how condition begins\'', '\'July 2, 2019\'', '\'University of North Carolina Health Care\'', '\'Scientists have uncovered details of a key cellular mechanism crucial for proper brain development. It involves a gene that, when mutated, had previously been linked to the development of autism.\n\'', '\'\nThe discovery, published in Neuron, illuminates the molecular details of a key process in brain development and adds to the scientific understanding of the biological basis of autism spectrum disorder (ASD), a condition linked to brain development and estimated to affect about one in 59 children born in the United States.\n\"This finding suggests that ASD can be caused by disruptions occurring very early on, when the cerebral cortex is just beginning to construct itself,\" said study senior author Eva S. Anton, PhD, professor of cell biology and physiology at the UNC School of Medicine and member of the UNC Neuroscience Center and the UNC Autism Research Center.\nThe cerebral cortex -- which in humans is responsible for higher brain functions including perception, speech, long-term memory, and consciousness -- is relatively large and dominant compared to other brain structures.\nHow the cortex constructs itself in the developing brain of a human or other mammal is far from fully understood. But scientists know that early in cortical development, precursor cells called radial glial cells (RGCs) appear at the bottom of the developing cortex in a regularly spaced or tiled pattern. Each RGC sprouts a single stalk-like structure, called a basal process that extends to the top of the cortex. Collectively these RGCs and their basal processes form a scaffold, much like the scaffolds of a construction site.\nRGCs divide to form young cortical neurons, and these baby neurons climb the scaffold to find their proper places in the developing brain. The cortex, thanks to this scaffolding system, normally develops a highly regular structure with six distinct layers of neurons required for the normal formation of functional neural cortical circuits.\nAnton and colleagues discovered that a gene encoding for a protein called Memo1 is needed to organize the tiled radial glial cell scaffold. Mutations in the Memo1 gene also have been found in some people with autism and are suspected of causing the condition. To explore Memo1\'s role in brain development and autism, Anton\'s team first engineered mice in which the Memo1 gene is deleted early in brain development in RGCs.\nThey found the resulting RGC scaffold is disrupted. Each RGC\'s stalk-like basal process formed too many branches and no longer forms a guiding scaffold, resulting in neuronal misplacement and disorganized layers. The scientists traced this ill effect, in part, to unstable microtubules, which normally help reinforce the scaffold structure and serve as railways for the internal traffic of key molecules necessary for RGC function.\nIntriguingly, studies of the brains of children with autism found patches of similar neuronal disorganization. The scientists then analyzed MEMO1 gene mutations reported recently in individuals with autism behaviors and intellectual disabilities. They discovered the human MEMO1 genetic mutation resulted in a shortened form of the Memo1 protein and this can disrupt RGC development\nFurther supporting the autism connection, Anton and his colleagues discovered the mice lacking Memo1 in their RGCs behaved abnormally, showing a lack of explorative activity similar to those seen in some people with autism.\nThe findings overall suggest that Memo1-associated autism may be wired into the brain very early in development than are other forms of autism with origins in disrupted neuronal differentiation and connectivity.\n\"For disorders of brain development such as ASD, it is important to understand the origins of the problem even if we are still far away from being able to correct developmental disruptions occurring in utero,\" Anton said. \"We need this foundational knowledge if we are to truly get to the root causes of these conditions and eventually develop better diagnostic or therapeutic strategies.\"\nAnton and colleagues are continuing to evaluate MEMO1 in cortical development and autism, and as more human mutations are being identified in this gene family and other ASD genes, they plan to shift from experiments in mice to the study of human brain organoids -- kind of mini brains that can be grown from patient derived stem cells with ASD related mutations.\nThe research was supported by grants from the National Institutes of Health (MH060929) and the National Institute of Neurological Disorders and Stroke (5P30NS045892-12).\nThe co-authors were Naoki Nakagawa PhD, Charlotte Plestant PhD, Keiko Yabuno-Nakagawa PhD, Jingjun Li PhD, Jason L. Stein PhD, all of UNC-Chapel Hill; Zoltan Molnar of University of Oxford, and Ali Badache PhD, of Centre de Recherche en Cancérologie de Marseille.\n\'', '\'Materials provided by University of North Carolina Health Care. Note: Content may be edited for style and length.\'', '\'\nNaoki Nakagawa, Charlotte Plestant, Keiko Yabuno-Nakagawa, Jingjun Li, Janice Lee, Chu-Wei Huang, Amelia Lee, Oleh Krupa, Aditi Adhikari, Suriya Thompson, Tamille Rhynes, Victoria Arevalo, Jason L. Stein, Zoltán Molnár, Ali Badache, E.S. Anton. Memo1-Mediated Tiling of Radial Glial Cells Facilitates Cerebral Cortical Development. Neuron, 2019; DOI: 10.1016/j.neuron.2019.05.049\n\n\'', '\'https://www.sciencedaily.com/releases/2019/07/190702112842.htm\n\'');
INSERT INTO `scidy` VALUES (33, '\'Atmosphere of midsize planet revealed by Hubble, Spitzer\'', '\'July 2, 2019\'', '\'NASA/Jet Propulsion Laboratory\'', '\'Two NASA space telescopes have identified the detailed chemical \'fingerprint\' of a planet between the sizes of Earth and Neptune. No planets like this can be found in our own solar system, but they are common around other stars.\n\'', '\'\nThe planet, Gliese 3470 b (also known as GJ 3470 b), may be a cross between Earth and Neptune, with a large rocky core buried under a deep, crushing hydrogen-and-helium atmosphere. Weighing in at 12.6 Earth masses, the planet is more massive than Earth but less massive than Neptune (which is more than 17 Earth masses).\nMany similar worlds have been discovered by NASA\'s Kepler space observatory, whose mission ended in 2018. In fact, 80% of the planets in our galaxy may fall into this mass range. However, astronomers have never been able to understand the chemical nature of such a planet until now, researchers say.\nBy inventorying the contents of GJ 3470 b\'s atmosphere, astronomers are able to uncover clues about the planet\'s nature and origin.\n\"This is a big discovery from the planet-formation perspective. The planet orbits very close to the star and is far less massive than Jupiter -- 318 times Earth\'s mass -- but has managed to accrete the primordial hydrogen/helium atmosphere that is largely \'unpolluted\' by heavier elements,\" said Björn Benneke of the University of Montreal in Canada. \"We don\'t have anything like this in the solar system, and that\'s what makes it striking.\"\nAstronomers enlisted the combined multi-wavelength capabilities NASA\'s Hubble and Spitzer space telescopes to do a first-of-a-kind study of GJ 3470 b\'s atmosphere.\nThis was accomplished by measuring the absorption of starlight as the planet passed in front of its star (transit) and the loss of reflected light from the planet as it passed behind the star (eclipse). All told, the space telescopes observed 12 transits and 20 eclipses. The science of analyzing chemical fingerprints based on light is called \"spectroscopy.\"\n\"For the first time we have a spectroscopic signature of such a world,\" said Benneke. But he is at a loss for classification: Should it be called a \"super-Earth\" or \"sub-Neptune?\" Or perhaps something else?\nFortuitously, the atmosphere of GJ 3470 b turned out to be mostly clear, with only thin hazes, enabling the scientists to probe deep into the atmosphere.\n\"We expected an atmosphere strongly enriched in heavier elements like oxygen and carbon which are forming abundant water vapor and methane gas, similar to what we see on Neptune,\" said Benneke. \"Instead, we found an atmosphere that is so poor in heavy elements that its composition resembles the hydrogen/helium-rich composition of the Sun.\"\nOther exoplanets, called \"hot Jupiters,\" are thought to form far from their stars and over time migrate much closer. But this planet seems to have formed just where it is today, said Benneke.\nThe most plausible explanation, according to Benneke, is that GJ 3470 b was born precariously close to its red dwarf star, which is about half the mass of our Sun. He hypothesizes that essentially it started out as a dry rock and rapidly accreted hydrogen from a primordial disk of gas when its star was very young. The disk is called a \"protoplanetary disk.\"\n\"We\'re seeing an object that was able to accrete hydrogen from the protoplanetary disk but didn\'t run away to become a hot Jupiter,\" said Benneke. \"This is an intriguing regime.\"\nOne explanation is that the disk dissipated before the planet could bulk up further. \"The planet got stuck being a sub-Neptune,\" said Benneke.\nNASA\'s upcoming James Webb Space Telescope will be able to probe even deeper into GJ 3470 b\'s atmosphere, thanks to Webb\'s unprecedented sensitivity in the infrared. The new results have already spawned great interest from American and Canadian teams developing the instruments on Webb. They will observe the transits and eclipses of GJ 3470 b at light wavelengths where the atmospheric hazes become increasingly transparent.\nThe Hubble Space Telescope is a project of international cooperation between NASA and ESA (European Space Agency). NASA\'s Goddard Space Flight Center in Greenbelt, Maryland, manages the telescope. The Space Telescope Science Institute (STScI) in Baltimore, Maryland, conducts Hubble science operations. STScI is operated for NASA by the Association of Universities for Research in Astronomy in Washington, D.C.\nThe Jet Propulsion Laboratory in Pasadena, California, manages the Spitzer Space Telescope mission for NASA\'s Science Mission Directorate in Washington. Science operations are conducted at the Spitzer Science Center at Caltech in Pasadena. Space operations are based at Lockheed Martin Space Systems in Littleton, Colorado. Data are archived at the Infrared Science Archive housed at IPAC at Caltech. Caltech manages JPL for NASA.\n\'', '\'Materials provided by NASA/Jet Propulsion Laboratory. Note: Content may be edited for style and length.\'', 'NULL', '\'https://www.sciencedaily.com/releases/2019/07/190702164603.htm\n\'');
INSERT INTO `scidy` VALUES (34, '\'\'Mystical\' psychedelic compound found in normal brains of rats\'', '\'June 27, 2019\'', '\'Michigan Medicine - University of Michigan\'', '\'A study in rats has revealed the presence of naturally occurring dimethyltryptamine, a hallucinogen.\n\'', '\'\nThe active ingredient responsible for these psychedelic visions is a molecule called dimethyltryptamine (DMT). For the first time, a team led by Michigan Medicine has discovered the widespread presence of naturally-occurring DMT in the mammalian brain. The finding is the first step toward studying DMT -- and figuring out its role -- within the brains of humans.\n\"DMT is not just in plants, but also can be detected in mammals,\" says Jimo Borjigin, Ph.D., of the Department of Molecular and Integrative Physiology. Her interest in DMT came about accidentally. Before studying the psychedelic, her research focused on melatonin production in the pineal gland.\nIn the seventeenth century, the philosopher Rene Descartes claimed that the pineal gland, a small pinecone-shaped organ located deep in the center of the brain, was the seat of the soul. Since its discovery, the pineal gland, known by some as the third eye, has been shrouded in mystery. Scientists now know it controls the production of melatonin, playing an important role in modulating circadian rhythms, or the body\'s internal clock. However, an online search for notes to include in a course she was teaching opened Borjigin\'s eyes to a thriving community still convinced of the pineal gland\'s mystical power.\nThe core idea seems to come from a documentary featuring the work of researcher Rick Strassman, Ph.D. with the University of New Mexico School of Medicine. In the mid-1990s, he conducted an experiment in which human subjects were given DMT by IV injection and interviewed after its effects wore off. In a documentary about the experiment, Strassman claims that he believed the pineal gland makes and secretes DMT.\n\"I said to myself, \'wait, I\'ve worked on the pineal gland for years and have never heard of this,\'\" she said. She contacted Strassman, requesting the source of his statement. When Strassman admitted that it was just a hypothesis, Borjigin suggested they work together to test it. \"I thought if DMT is an endogenous monoamine, it should be very easy to detect using a fluorescence detector.\"\nUsing a process in which microdialysis tubing is inserted into a rat brain through the pineal gland, the researchers collected a sample that was analyzed for -- and confirmed -- the presence of DMT. That experiment resulted in a paper published in 2013.\nHowever, Borjigin was not satisfied. Next, she sought to discover how and where DMT was synthesized. Her graduate student, Jon Dean, lead author of the paper, set up an experiment using a process called in situ hybridization, which uses a labeled complementary strand of DNA to localize a specific RNA sequence in a tissue section.\n\"With this technique, we found brain neurons with the two enzymes required to make DMT,\" says Borjigin. And they were not just in the pineal gland.\n\"They are also found in other parts of the brain, including the neocortex and hippocampus that are important for higher-order brain functions including learning and memory.\"\nThe results are published in the journal Scientific Reports.\nHer team\'s work has also revealed that the levels of DMT increase in some rats experiencing cardiac arrest. A paper published in 2018 by researchers in the U.K. purported that DMT simulates the near death experience, wherein people report the sensation of transcending their bodies and entering another realm. Borjigin hopes to probe further to discover the function of naturally occurring levels of DMT in the brain -- and what if any role it plays in normal brain functions.\n\"We don\'t know what it\'s doing in the brain. All we\'re saying is we discovered the neurons that make this chemical in the brain, and they do so at levels similar to other monoamine neurotransmitters.\"\n\'', '\'Materials provided by Michigan Medicine - University of Michigan. Original written by Kelly Malcom. Note: Content may be edited for style and length.\'', '\'\nJon G. Dean, Tiecheng Liu, Sean Huff, Ben Sheler, Steven A. Barker, Rick J. Strassman, Michael M. Wang, Jimo Borjigin. Biosynthesis and Extracellular Concentrations of N,N-dimethyltryptamine (DMT) in Mammalian Brain. Scientific Reports, 2019; 9 (1) DOI: 10.1038/s41598-019-45812-w\n\n\'', '\'https://www.sciencedaily.com/releases/2019/06/190627113951.htm\n\'');
INSERT INTO `scidy` VALUES (35, '\'Wood products mitigate less than one percent of global carbon emissions\'', '\'July 1, 2019\'', '\'University of Wisconsin-Madison\'', '\'The world\'s wood products -- all the paper, lumber, furniture and more -- offset just one percent of annual global carbon emissions by locking away carbon in woody forms, according to new research.\n\'', '\'\nAn analysis across 180 countries found that global wood products offset 335 million tons of carbon dioxide in 2015, 71 million tons of which were unaccounted for under current United Nations standards. Wood product carbon sequestration could rise more than 100 million tons by 2030, depending on the level of global economic growth.\nThe results provide countries with the first consistent look at how their timber industries could offset their carbon emissions as nations search for ways to keep climate change manageable by severely curbing emissions.\nYet the new research also highlights how wood products account for just a small fraction of the needed offsets for all but a select few timber-heavy countries.\nCraig Johnston, a professor of forest economics at the University of Wisconsin-Madison, and Volker Radeloff, a UW-Madison professor of forest and wildlife ecology, published their findings July 1 in the Proceedings of the National Academy of Sciences.\n\"Countries are looking for net-negative emissions strategies. So it\'s not just about lowering our emissions but pursuing strategies that might have storage potential, and harvested wood products are one of those options,\" says Johnston. \"It\'s nice because you can pursue options that don\'t hinder growth. The question is, can we continue to consume wood products and have climate change benefits associated with that consumption?\"\nTo address that question, Johnston worked with Radeloff to develop a consistent, international analysis of the carbon storage potential of these products, which countries must now account for under the global Paris Agreement to reduce carbon emissions.\nThey used data on lumber harvests and wood product production from 1961 to 2015, the most recent year available, from the U.N. Food and Agriculture Organization. The researchers modeled future carbon sequestration in wood products using five broad models of possible economic and population growth, the two factors that most affect demand for these products.\nAlthough the production of wood products in 2015 offset less than 1 percent of global carbon emissions, the proportion was much higher for a handful of countries with large timber industries. Sweden\'s pool of wood products, for example, offset 9 percent of the country\'s carbon emissions in 2015, which accounted for 72 percent of emissions from industrial sources that year.\nBut for most countries, including the U.S., wood products mitigated a much smaller fraction of overall emissions in 2015, and this proportion is not expected to increase significantly through 2065, the researchers found.\nCurrent U.N. guidelines only allow countries to count the carbon stored in wood products created from domestic timber harvests, not the timber grown locally and shipped internationally, nor products produced from imported lumber. These regulations create a gap between the actual amount of carbon stored in the world\'s wood products and what is officially counted.\nIn 2015, that gap amounted to 71 million tons of carbon dioxide, equivalent to the emissions from 15 million cars. If those guidelines remain unchanged, by 2065 another 50 million tons of carbon dioxide may go unaccounted for due to this gap. But this additional, uncounted carbon does not significantly increase the proportion of global emissions offset by wood products.\nJohnston and Radeloff also found that the level of carbon stored in wood products is extremely sensitive to economic conditions. Slow or negative growth could significantly reduce the amount of carbon offset by these industries.\n\"As wood products are produced, you\'re adding to this carbon pool in the country, but these products do eventually decay. There\'s carbon emissions today from furniture or lumber that was produced 50 or 75 years ago,\" says Johnston. \"So if we\'re not producing at a rate that at least offsets those emissions, then we\'ll actually see that carbon pool become a net source of emissions.\"\nFor example, the Great Recession in 2008 and 2009 turned America\'s wood products from a net sink of carbon into a net emitter. A similar effect released millions of tons of carbon dioxide from wood products for years after the Soviet Union collapsed, Johnston and Radeloff found.\nAll five of the study\'s projections for future economic growth predict that more carbon will be captured in wood products, but unforeseen economic shocks could temporarily reverse that trend for particular countries.\nThe current study offers a chance to assess current obligations and help countries predict future emissions. The results may also inform the next round of emissions targets and negotiations, the researchers say.\n\"We\'re making these data public. The whole model for all countries, for all wood products, for all scenarios is available,\" says Johnston. \"Now we know what it looks like for every country under a common model and common assumptions moving forward.\"\n\'', '\'Materials provided by University of Wisconsin-Madison. Note: Content may be edited for style and length.\'', '\'\nCraig M. T. Johnston, Volker C. Radeloff. Global mitigation potential of carbon stored in harvested wood products. Proceedings of the National Academy of Sciences, 2019; 201904231 DOI: 10.1073/pnas.1904231116\n\n\'', '\'https://www.sciencedaily.com/releases/2019/07/190701163837.htm\n\'');
INSERT INTO `scidy` VALUES (36, '\'Nerve transfer surgery restores hand function and elbow extension in 13 young adults with complete paralysis\'', '\'July 4, 2019\'', '\'The Lancet\'', '\'Nerve transfer surgery has enabled 13 young adults with complete paralysis to regain movement and function in their elbows and hands, according to the largest case series of this technique in people with tetraplegia (paralysis of both the upper and lower limbs).\n\'', '\'\nDuring the surgery, Australian surgeons attached functioning nerves above the spinal injury to paralysed nerves below the injury. Two years after surgery, and following intensive physical therapy, participants were able to reach their arm out in front of them and open their hand to pick up and manipulate objects. Restoring elbow extension improved their ability to propel their wheelchair and to transfer into bed or a car.\nThey can now perform everyday tasks independently such as feeding themselves, brushing teeth and hair, putting on make-up, writing, handling money and credit cards, and using tools and electronic devices.\nThe findings suggest that nerve transfers can achieve similar functional improvements to traditional tendon transfers, with the benefit of smaller incisions and shorter immobilisation times after surgery.\nIn 10 participants, nerve transfers were uniquely combined with tendon transfers allowing different styles of reconstruction to be performed in each hand, and enabling participants to benefit from the innate strengths of both tendon and nerve transfers. Nerve transfers restored more natural movement and finer motor control in one hand, and tendon transfers restored more power and heavy lifting ability in the other hand.\nWhile only a small study, researchers say that nerve transfers are a major advance in the restoration of hand and arm function, and offer another safe, reliable surgical option for people living with tetraplegia.\nNevertheless, four nerve transfers failed in three participants and the authors conclude that more research will be needed to determine which people are the best candidates to select for nerve transfer surgery to minimise the incidence of failure.\n\"For people with tetraplegia, improvement in hand function is the single most important goal. We believe that nerve transfer surgery offers an exciting new option, offering individuals with paralysis the possibility of regaining arm and hand functions to perform everyday tasks, and giving them greater independence and the ability to participate more easily in family and work life,\" says Dr Natasha van Zyl from Austin Health in Melbourne, Australia who led the research.\n\"What\'s more, we have shown that nerve transfers can be successfully combined with traditional tendon transfer techniques to maximise benefits. When grasp and pinch was restored using nerve transfers in one hand and tendon transfers in the other, participants consistently reporting that they liked both hands for different reasons and would not choose to have two hands reconstructed in the same way.\"\nTraditionally, upper limb function has been reconstructed using tendon transfer surgery, during which muscles that still work, but are designed for another function, are surgically re-sited to do the work of muscles that are paralysed. In contrast, nerve transfers allow the direct reanimation of the paralysed muscle itself. Additionally, nerve transfers can re-animate more than one muscle at a time, have a shorter period of immobilisation after surgery (10 days in a sling vs 6-12 weeks in a brace for a nerve transfer for elbow extension), and avoid the technical problems associated with of tendon transfer surgery including tendon tensioning during surgery and mechanical failure (stretch or rupture) after surgery.\nPrevious single case reports and small retrospective studies have shown nerve transfer surgery to be feasible and safe in people with tetraplegia. But this is the first prospective study to use standardised functional outcome measures and combinations of multiple nerve and tendon transfer surgeries.\nIn total the study recruited 16 young adults (average age 27 years) with traumatic, early (less than 18 months post injury) spinal cord injury to the neck (C5-C7), who were referred to Austin Health in Melbourne for restoration of function in the upper limb. Most were the result of motor vehicle accidents or sports injuries.\nParticipants underwent single or multiple nerve transfers in one or both upper limbs to restore elbow extension, grasp, pinch, and hand opening. This involved taking working nerves to expendable muscles innervated above the spinal injury and attaching them to the nerves of paralysed muscles innervated below the injury to restore voluntary control and reanimate the paralysed muscle.\nFor example, the surgeons selected the nerve supplying the teres minor muscle in the shoulder as a donor nerve and attached it to the nerve supplying the triceps that activates the muscles that extend (straighten) the elbow. To restore grasp and pinch the nerve to a spare wrist extensor muscle was transferred to the anterior interosseous nerve.\nIn total, 59 nerve transfers were completed in 16 participants (13 men and three women; 27 limbs). In 10 participants (12 limbs), nerve transfers were combined with tendon transfers to improve hand function.\nParticipants completed assessments on their level of independence related to activities of daily living (e.g., self-care, toilet, upper limb function, muscle power, grasp and pinch strength, and hand opening ability) before surgery, one year after surgery, and again two years later. Two participants were lost to follow up, and there was one death (unrelated to the surgery).\nAt 24 months, significant improvements were noted in the hands ability to pick up and release several objects within a specified time frame and independence. Prior to surgery, none of the participants were able to score on the grasp or pinch strength tests, but 2 years later pinch and grasp strength were high enough to perform most activities of daily living.\nThree participants had four failed nerve transfers -- two had a permanent decrease in sensation, and two had a temporary decrease in wrist strength that resolved by 1 year after surgery. Overall, surgery was well tolerated. Five serious adverse events were recorded (including a fall from a wheelchair with femur fracture), but none were related to the surgery.\nDespite these achievements, nerve transfer surgery still has some limitations. For the best results nerve transfers should ideally be performed within 6-12 months of injury. Additionally, it can take months after nerve transfer for nerve regrowth into the paralysed muscle to occur and for new movement to be seen, and years until full strength is achieved. However, the authors note that one of the benefits of nerve transfers is that most movements not successfully restored by nerve transfers can still be restored using tendon transfers.\nDiscussing the implications of the findings in a linked comment, Dr Ida Fox from Washington University in the USA writes, \"Stem cells and neuroprostheses could change the landscape of regenerative medicine in the future. For now, nerve transfers are a cost-effective way to harness the body\'s innate capability to restore movement in a paralysed limb. As nerve transfers are adopted and their uses adapted, careful ongoing outcomes research -- including comparison of nerve versus tendon transfer outcomes, which nerve transfers produce the greatest functional improvements, and optimal timings for surgery after injury -- is paramount to advancing the field. Detailed study of the reasons for nerve transfer failure is also required, as is improving our understanding of the effects of biopsychosocial factors (including access to information and care, psychological readiness, and social support) on patient decision making and outcomes.\"\n\'', '\'Materials provided by The Lancet. Note: Content may be edited for style and length.\'', '\'\nNatasha van Zyl, Bridget Hill, Catherine Cooper, Jodie Hahn, Mary P Galea. Expanding traditional tendon-based techniques with nerve transfers for the restoration of upper limb function in tetraplegia: a prospective case series. The Lancet, 2019; DOI: 10.1016/S0140-6736(19)31143-2\n\n\'', '\'https://www.sciencedaily.com/releases/2019/07/190704191425.htm\n\'');
INSERT INTO `scidy` VALUES (37, '\'Preventing hereditary deafness\'', '\'July 3, 2019\'', '\'Harvard Medical School\'', '\'An optimized version of the CRISPR-Cas9 gene-editing system prevents hearing loss with no detectable off-target effects in so-called Beethoven mice, which carry a mutation that causes profound hearing loss in humans and mice alike. Results offer proof of principle for using the same gene-editing technique for other inherited human genetic diseases.\n\'', '\'\nThe animals -- known as Beethoven mice -- were treated for the same genetic mutation that causes progressive hearing loss in humans, culminating in profound deafness by their mid-20s.\nThe new approach, described online July 3 in Nature Medicine , involves an optimized, more precise version of the classic CRISPR-Cas9 gene-editing system that is better at recognizing the disease-causing mutation seen in Beethoven mice. The refined tool allowed scientists to selectively disable the defective copy of a hearing gene called Tmc1, while sparing the healthy copy.\nNotably, the researchers report, their system managed to recognize a single incorrect DNA letter in the defective copy among 3 billion letters in the mouse genome.\nMuch more work remains to be done before even a highly precise gene-editing therapy like this one could be used in humans, the researchers cautioned. However, they said, the work represents a milestone because it greatly improves the efficacy and safety of standard gene-editing techniques.\n\"Our results demonstrate that this more refined, better targeted version of the now-classic CRISPR/Cas9 editing tool achieves an unprecedented level of identification and accuracy,\" said study co-senior investigator David Corey, the Bertarelli Professor of Translational Medical Science in the Blavatnik Institute at Harvard Medical School.\nFurthermore, the team said, the results set the stage for using the same precision approach to treat other dominantly inherited genetic diseases that arise from a single defective copy of a gene.\nEveryone inherits two copies of the same gene -- one from each parent. In many cases, one normal gene is sufficient to ensure normal function that spares the individual from disease. By contrast, in so-called dominantly inherited genetic disorders, a single defective copy can cause illness.\n\"We believe our work opens the door toward a hyper-targeted way to treat an array of genetic disorders that arise from one defective copy of a gene,\" said study co-senior investigator Jeffrey Holt, Harvard Medical School professor of otolaryngology and neurology at Boston Children\'s Hospital, who is also affiliated with the F.M. Kirby Neurobiology Center at Boston Children\'s. \"This truly is precision medicine.\"\nThe mice carrying the faulty Tmc1 gene are known as Beethoven mice because the course of their disease mimics the progressive hearing loss experienced by the famed composer. The cause of Ludwig van Beethoven\'s deafness, however, remains a matter of speculation.\nIn mice, the Beethoven defect is marked by one incorrect letter in the DNA sequence of the Tmc1 gene -- an A instead of a T -- a single error that spells the difference between normal hearing and deafness.\nDisabling, or silencing, the mutant copy of the Tmc1 gene would be sufficient to preserve the animal\'s hearing, but how could it be done without inadvertently disabling the healthy gene as well?\nTwo keys are better than one\nClassic CRISPR-Cas9 gene editing systems work by using a guiding molecule -- gRNA -- to identify the target mutant DNA sequence. Once the target DNA is pinpointed, the cutting enzyme -- Cas9 -- snips it.\nSo far, these gene editors have shown less-than-perfect accuracy. This is because the guide RNA that leads the Cas9 enzyme to the target site and the Cas9 enzyme that cuts the target DNA are not entirely precise and could end up cutting the wrong DNA.\nTo circumvent these challenges, researchers adapted a tool originally developed by Keith Joung, HMS professor of pathology, and Ben Kleinstiver, HMS assistant professor of pathology, at Massachusetts General Hospital, which uses a modified Cas9 enzyme derived from Staphylococcus aureus instead of the standard Cas9 that is derived from the bacterium Streptococcus pyogenes.\nTo achieve enhanced accuracy of the detection and disruption, the new, optimized system combines two levels of recognition -- gRNA to locate the target gene and a modified form of Cas9 that can pinpoint the specific DNA mutation in Beethoven mice. The use of two forms of identification ensures the precise and selective cutting of the aberrant copy -- and only the aberrant copy -- of that gene.\n\"We took advantage of the fact that this system recognizes mutant DNA but not normal DNA and uses a dual recognition system for enhanced precision,\" said study first author Bence Gyorgy, who conducted the work while at Harvard Medical School and is now at the Institute of Molecular and Clinical Ophthalmology in Basel, Switzerland. \"This approach resulted in an unprecedented level of specificity in targeting the mutant gene.\"\nIn an initial set of experiments in cells with and without the Beethoven mutation, the tool accurately distinguished between mutant DNA and normal DNA in copies of the Tmc1 gene. Further analysis revealed that in Beethoven cells, which contained one defective and one normal copy of the gene, at least 99 percent of the molecular \"cuts\" occurred exclusively in the defective copy of the gene.\nNext, researchers injected the gene-editing treatment into the inner ears of mice with and without the Beethoven mutation. DNA analysis showed that editing activity occurred only in the inner ear cells of mice with the Beethoven defect. No editing changes were detected in cells from the inner ears of treated mice that didn\'t have the mutation -- a finding that confirmed the tool\'s precision.\nTo determine whether the gene-editing therapy interfered with normal gene function, the scientists stimulated hearing cells -- called hair cells -- from the inner ears of treated mice that didn\'t carry the Beethoven defect. The cells showed unchanged, normal hearing responses, affirming that the gene-editing therapy had no effect on normal gene function.\nSilencing Beethoven\nTo measure whether the therapy worked in animals rather than just in cells, researchers performed the gold-standard test for hearing. They measured the animals\' auditory brainstem responses, which capture how much sound is detected by hair cells in the inner ear and transmitted to the brain.\nWithout treatment, Beethoven mice typically are completely deaf by 6 months of age. By comparison, mice without the genetic defect retain normal hearing throughout life and can detect sounds at around 30 decibels -- a level similar to a whisper.\nTwo months after receiving the gene-editing therapy, Beethoven mice exhibited markedly better hearing than untreated siblings carrying the genetic mutation. The treated animals were capable of detecting sounds at about 45 decibels -- the level of a normal conversation -- or about 16 times quieter than untreated mice. The Beethoven mouse with the greatest hearing preservation was capable of hearing sounds at 25 to 30 decibels, virtually indistinguishable from its healthy peers.\nTaken together, the findings demonstrate that the novel gene therapy effectively silenced the defective copy of the gene and salvaged the animals\' hearing from the rapid demise typically seen in the disease.\nBecause the disease is marked by progressive hearing loss, the researchers assessed the effect of therapy on the progression over several months. Researchers administered treatment shortly after birth and tested hearing levels in treated and untreated mice with and without the mutation every four weeks for up to six months. In month one, untreated Beethoven mice could hear low-frequency sounds but had notable hearing loss at high frequencies. By month six after birth, untreated Beethoven mice had lost all their hearing. In contrast, treated Beethoven mice retained near-normal hearing at low frequencies, with some showing near-normal hearing even at high frequencies.\nNotably, treated animals that didn\'t carry the genetic defect did not experience any hearing loss as a result of the gene therapy -- a finding that demonstrated the safety of the procedure and its ability to selectively target the aberrant copy of the gene. Even more encouragingly, a small subset of treated Beethoven mice that were followed for nearly a year retained stable, near-normal hearing.\nBecause the Beethoven defect is marked by the progressive deterioration and death of hearing cells in the inner ear, the researchers used electron microscopy to visualize the structure of these critical hearing cells. As expected, in the untreated Beethoven mice, the researchers saw gradual loss of hearing cells along with deterioration in their structure. By contrast, treated Beethoven mice and treated healthy mice both retained a normal number of hearing cells with intact or near-intact structure.\nIn a final experiment, the scientists tested the effect of the treatment in a line of human cells carrying the Beethoven mutation. DNA analysis revealed that treatment caused editing exclusively in the mutant copy of the Tmc1 gene and spared the normal one.\nBecause of its ability to target single-point genetic mutations, the approach holds promise for 15 other forms of inherited deafness also caused by a single-letter mutation in the DNA sequence of other hearing genes.\nAdditionally, the team said, their technique could be adapted for use in other dominantly inherited genetic disease caused by single-point mutations. To determine its hypothetical utility, the scientists scanned the federal ClinVar database -- a national repository of all known genetic mutations linked to human diseases. The analysis showed that based on the tool\'s specificity, it could correctly identify 3,759 defective gene variants collectively responsible for one-fifth of dominant human genetic mutations.\n\"To be sure, this is the first step in a long journey,\" Holt said. \"But what we have here is proof of principle that demonstrates this highly specific, highly targeted treatment could be developed to selectively silence genes that carry single-point mutations and potentially treat many other forms of human disease.\"\n\'', '\'Materials provided by Harvard Medical School. Original written by Ekaterina Pesheva. Note: Content may be edited for style and length.\'', '\'\nBence György, Carl Nist-Lund, Bifeng Pan, Yukako Asai, K. Domenica Karavitaki, Benjamin P. Kleinstiver, Sara P. Garcia, Mikołaj P. Zaborowski, Paola Solanes, Sofia Spataro, Bernard L. Schneider, J. Keith Joung, Gwenaëlle S. G. Géléoc, Jeffrey R. Holt, David P. Corey. Allele-specific gene editing prevents deafness in a model of dominant progressive hearing loss. Nature Medicine, 2019; DOI: 10.1038/s41591-019-0500-9\n\n\'', '\'https://www.sciencedaily.com/releases/2019/07/190703121434.htm\n\'');
INSERT INTO `scidy` VALUES (38, '\'Pain signaling in humans more rapid than previously known\'', '\'July 4, 2019\'', '\'Linköping University\'', '\'Pain signals can travel as fast as touch signals, according to a new study. The discovery of a rapid pain-signaling system challenges our current understanding of pain.\n\'', '\'\nIt has until now been believed that nerve signals for pain are always conducted more slowly than those for touch. The latter signals, which allow us to determine where we are being touched, are conducted by nerves that have a fatty sheath of myelin that insulates the nerve. Nerves with a thick layer of myelin conduct signals more rapidly than unmyelinated nerves. In contrast, the signalling of pain in humans has been thought to be considerably slower and carried out by nerves that have only a thin layer of myelin, or none at all.\nIn monkeys and many other mammals, on the other hand, part of the pain-signalling system can conduct nerve signals just as fast as the system that signals touch. The scientists speculated whether such a system is also present in humans.\n\"The ability to feel pain is vital to our survival, so why should our pain-signalling system be so much slower than the system used for touch, and so much slower than it could be?\" asks Saad Nagi, principal research engineer of the Department of Clinical and Experimental Medicine and the Center for Social and Affective Neuroscience (CSAN) at Linköping University.\nTo answer this, the scientists used a technique that allowed them to detect the signals in the nerve fibres from a single nerve cell. They examined 100 healthy volunteers and looked for nerve cells that conducted signals as rapidly as the nerve cells that detect touch, but that had the properties of pain receptors, otherwise known as nociceptors. Pain receptors are characterised by the ability to detect noxious stimuli, such as pinching and abrasion of the skin, while not reacting to light touch. The researchers found that 12% of thickly myelinated nerve cells had the same properties as pain receptors, and in these nerve cells the conduction speed was as high as in touch-sensitive nerve cells.\nThe next step of the scientists\' research was to determine the function of these ultrafast pain receptors. By applying short electrical pulses through the measurement electrodes, they could stimulate individual nerve cells. The volunteers described that they experienced sharp or pinprick pain.\n\"When we activated an individual nerve cell, it caused a perception of pain, so we conclude that these nerve cells are connected to pain centres in the brain,\" says Saad Nagi.\nThe research team also investigated patients with various rare neurological conditions. One group of people had, as adults, acquired nerve damage that led to the thickly myelinated nerve fibres being destroyed, while the small fibres were spared. These patients cannot detect light touch. The scientists predicted that the loss of myelinated nerve fibres should also affect the rapidly conducting pain system they had identified. It turned out that these people had an impaired ability to experience mechanical pain. Examination of patients with two other rare neurological conditions gave similar results. These results may be highly significant for pain research, and for the diagnosis and care of patients with pain.\n\"It\'s becoming evident that thickly myelinated nerve fibres contribute to the experience of pain when it has a mechanical cause. Our results challenge the textbook description of a rapid system for signalling touch and a slower system for signalling pain. We suggest that pain can be signalled just as rapidly as touch,\" says Saad Nagi.\n\'', '\'Materials provided by Linköping University. Note: Content may be edited for style and length.\'', '\'\nSaad S. Nagi, Andrew G. Marshall, Adarsh Makdani, Ewa Jarocka, Jaquette Liljencrantz, Mikael Ridderström, Sumaiya Shaikh, Francis O’Neill, Dimah Saade, Sandra Donkervoort, A. Reghan Foley, Jan Minde, Mats Trulsson, Jonathan Cole, Carsten G. Bönnemann, Alexander T. Chesler, M. Catherine Bushnell, Francis McGlone, Håkan Olausson. An ultrafast system for signaling mechanical pain in human skin. Science Advances, 2019; 5 (7): eaaw1297 DOI: 10.1126/sciadv.aaw1297\n\n\'', '\'https://www.sciencedaily.com/releases/2019/07/190704191429.htm\n\'');
INSERT INTO `scidy` VALUES (39, '\'Researchers map crystals to advance treatments for stroke, diabetes, dementia\'', '\'July 3, 2019\'', '\'West Virginia University\'', '\'A team of researchers have mapped the crystal structure of a protein called \'mitoNEET\' and pinpointed how a drug latches on it.\n\'', '\'\nResearchers at West Virginia University have mapped the crystal structure of a protein that resides in our cells and determined -- for the first time -- how a drug latches onto it. The findings appear in Communications Chemistry, a Nature research journal.\nThe study -- funded by the West Virginia Clinical and Translational Science Institute -- centered on a protein called \"mitoNEET.\" MitoNEET inhabits the outer membrane of our mitochondria, which act like power plants that energize our cells.\n\"MitoNEET is a novel therapeutic target for metabolic-based diseases and could possibly lead to disease-modifying treatments for Alzheimer\'s disease and stroke,\" said Werner Geldenhuys, an associate professor in the School of Pharmacy and School of Medicine. He and his colleagues -- including Aaron Robart, an assistant professor in the WVU School of Medicine, John Hollander, assistant dean for professional programs in the WVU School of Medicine, and Timothy Long, an associate professor in the Marshall University School of Pharmacy -- carried out the project.\n\"This protein has been implicated in a lot of diseases that are very tough to tackle: things like diabetes, stroke, heart disease,\" Robart said. \"We don\'t actually know what the protein does yet, but it hangs out in proximity to the powerhouse of the cell, and all of these diseases have an energy-flow theme to them.\"\nTo explore the role mitoNEET plays in our energy processes, the researchers isolated mitoNEET from both bacterial overexpression and animal models. Then they synthesized 11 molecules similar to furosemide -- a common diuretic sold under the brand name LASIX -- and exposed the mitoNEET to them.\nAfter the molecules bonded to the mitoNEET, the researchers built atom-by-atom maps of the pairings. They remotely controlled Argonne National Laboratory\'s Advanced Photon Source -- which bombards samples with ultra-bright, high-energy X-rays -- to reveal precisely how the molecules came together.\nThe team discovered that the molecules docked into a cluster of iron and sulfur atoms that made up part of the protein. Raisa Nuñez, an undergraduate participating in the Research Apprenticeship Program, collected preliminary structural data. \"This highlights that significant scientific discovery can come at any career level,\" Robart said.\n\"These findings are of importance as they allow us to continue to understand the role played by mitochondria and bioenergetics in many disease states,\" Hollander said. \"The modulation of mitochondrial function through targeted therapeutics may be a critical avenue of drug discovery.\"\nUnderstanding mitoNEET\'s cellular function could improve the performance of drugs that work by altering the protein\'s activity. For example, adding an extra oxygen group to a drug\'s molecular structure could dramatically tighten its bond to mitoNEET and eliminate unintended binding to other cellular proteins.\nThe potential upshot for patients who take the drug? Better symptom relief.\n\"The success of this project really illustrates how approaches that are considered basic science can provide considerable insight into clinical problems,\" said Michael Schaller, who chairs the School of Medicine\'s Department of Biochemistry. \"It also demonstrates the power of tackling problems as teams consisting of members with very different expertise.\"\n\'', '\'Materials provided by West Virginia University. Note: Content may be edited for style and length.\'', '\'\nWerner J. Geldenhuys, Timothy E. Long, Pushkar Saralkar, Toshio Iwasaki, Raisa A. A. Nuñez, Rajesh R. Nair, Mary E. Konkle, Michael A. Menze, Mark V. Pinti, John M. Hollander, Lori A. Hazlehurst, Aaron R. Robart. Crystal structure of the mitochondrial protein mitoNEET bound to a benze-sulfonide ligand. Communications Chemistry, 2019; 2 (1) DOI: 10.1038/s42004-019-0172-x\n\n\'', '\'https://www.sciencedaily.com/releases/2019/07/190703171851.htm\n\'');
INSERT INTO `scidy` VALUES (40, '\'Imprinted spheres fight breast cancer\'', '\'July 3, 2019\'', '\'Wiley\'', '\'A particularly aggressive, metastasizing form of cancer, HER2-positive breast cancer, may be treated with nanoscopic particles \'\'imprinted\'\' with specific binding sites for the receptor molecule HER2. The selective binding of the nanoparticles to HER2 significantly inhibits multiplication of the tumor cells.\n\'', '\'\nBreast cancer is the most common form of cancer in women and one of the leading causes of death. About 20 to 30 % of breast cancer cases involve the very poorly treatable HER2-positive variety. HER2 stands for Human Epidermal Growth Factor Receptor 2, a protein that recognizes and binds to a specific growth factor. HER2 spans across the cell membrane: one part protrudes into the interior of the cell; the other is on the cell surface. As soon as a growth factor docks, the extracellular parts of HER2 bind into a heterodimer with a second, closely related HER, such as HER1 or HER3. This triggers a multistep signal cascade within the cell, which is critically involved in processes like cell division, metastasis, and the formation of blood vessels that supply the tumor. HER2-positive tumor cells contain significantly higher concentrations of HER2. One current therapy for early-stage HER2-positive tumors is based on binding an antibody to HER2 to block the dimerization. Researchers led by Zhen Liu at Nanjing University (China) have now developed \"molecularly imprinted\" biocompatible polymer nanoparticles that recognize HER2 just as specifically as an antibody in order to prevent the dimerization.\nNanoparticles can be molecularly imprinted in that -- to simplify -- a polymerizable mixture is polymerized into nanospheres in the presence of the (bio)molecules they are supposed to recognize later. The (bio)molecules act as a kind of stamp, leaving nanoscopic \"imprints\" in the spheres. These then perfectly fit the molecules they were imprinted with and bind to them specifically. In contrast to antibodies, the nanospheres are easy and inexpensive to produce and are chemically stable.\nFor the imprinting process, the researchers use a special method (boronate affinity controllable oriented surface imprinting) that is particularly controllable and makes it possible to imprint using chains of sugar building blocks (glycans) as templates. Many proteins contain specific \"sugar chains.\" These are unique, like a protein fingerprint. The researchers used this kind of glycan from the extracellular end of the HER2 proteins as their \"stamp.\" This allowed them to produce imprinted nanoparticles that specifically recognize HER2 and selectively bind to it, inhibiting the dimerization. They were thus able to significantly reduce the multiplication of tumor cells in vitro and the growth of tumors in mice. In contrast, healthy cells were essentially unaffected.\n\'', '\'Materials provided by Wiley. Note: Content may be edited for style and length.\'', '\'\nYueru Dong, Wei Li, Zikuan Gu, Rongrong Xing, Yanyan Ma, Qi Zhang, Zhen Liu. Inhibition of HER2-Positive Breast Cancer Growth by Blocking the HER2 Signaling Pathway with HER2-Glycan-Imprinted Nanoparticles. Angewandte Chemie International Edition, 2019; DOI: 10.1002/anie.201904860\n\n\'', '\'https://www.sciencedaily.com/releases/2019/07/190703121429.htm\n\'');
INSERT INTO `scidy` VALUES (41, '\'World first:  Homing instinct applied to stem cells show cells \'home\' to cardiac tissue\'', '\'July 3, 2019\'', '\'University of Bristol\'', '\'In a world first, scientists have found a new way to direct stem cells to heart tissue. The findings could radically improve the treatment for cardiovascular disease, which causes more than a quarter of all deaths in the UK (1).\n\'', '\'\nTo date, trials using stem cells, which are taken and grown from the patient or donor and injected into the patient\'s heart to regenerate damaged tissue, have produced promising results.\nHowever, while these next generation cell therapies are on the horizon, significant challenges associated with the distribution of the stem cells have remained. High blood flow in the heart combined with various \'tissue sinks\', that circulating cells come into contact with, means the majority of the stem cells end up in the lungs and spleen.\nNow, researchers from Bristol\'s School of Cellular and Molecular Medicine have found a way to overcome this by modifying stem cells with a special protein so they \'home\' to heart tissue.\nDr Adam Perriman, the study\'s lead author, Associate Professor in Biomaterials, UKRI Future Leaders Fellow and founder of the cell therapy technology company CytoSeek, explained: \"With regenerative cell therapies, where you are trying to treat someone after a heart attack, the cells rarely go to where you want them to go. Our aim is to use this technology to re-engineer the membrane of cells, so that when they\'re injected, they\'ll home to specific tissues of our choice.\n\"We know that some bacterial cells contain properties that enable them to detect and \'home\' to diseased tissue. For example, the oral bacterial found in our mouths can occasionally cause strep throat. If it enters the blood stream it can \'home\' to damaged tissue in the heart causing infective endocarditis. Our aim was to replicate the homing ability of bacteria cells and apply it to stem cells.\"\nThe team developed the technology by looking at how bacterial cells use a protein called an adhesin to \'home\' to heart tissue. Using this theory, the researchers were able to produce an artificial cell membrane binding version of the adhesin that could be \'painted\' on the outside of the stem cells. In an animal model, the team were able to demonstrate that this new cell modification technique worked by directing stem cells to the heart in a mouse.\nDr Perriman added: \"Our findings demonstrate that the cardiac homing properties of infectious bacteria can be transferred to human stem cells. Significantly, we show in a mouse model that the designer adhesin protein spontaneously inserts into the plasma membrane of the stem cells with no cytotoxity, and then directs the modified cells to the heart after transplant. To our knowledge, this is the first time that the targeting properties of infectious bacteria have been transferred to mammalian cells.\n\"This new technique carries enormous potential for the seven million people currently living with heart disease in the UK.\"\nDr Perriman\'s UKRI Future Leaders fellowship is based on research funded by the Elizabeth Blackwell Institute-funded Catalyst project. He is also a member of the University\'s BrisSynBio, a multi-disciplinary research centre part of the Bristol BioDesign Institute, that focuses on the biomolecular design and engineering aspects of synthetic biology.\nDr Perriman is well-known for his pioneering research on the construction and study of novel synthetic biomolecular systems for regenerative engineering.\n\'', '\'Materials provided by University of Bristol. Note: Content may be edited for style and length.\'', '\'\nWenjin Xiao, Thomas I. P. Green, Xiaowen Liang, Rosalia Cuahtecontzi Delint, Guillaume Perry, Michael S. Roberts, Kristian Le Vay, Catherine R. Back, Raimomdo Ascione, Haolu Wang, Paul R. Race, Adam W. Perriman. Designer artificial membrane binding proteins to direct stem cells to the myocardium. Chemical Science, 2019; DOI: 10.1039/C9SC02650A\n\n\'', '\'https://www.sciencedaily.com/releases/2019/07/190703121425.htm\n\'');
INSERT INTO `scidy` VALUES (42, '\'Super-resolution microscopy illuminates associations between chromosomes\'', '\'July 3, 2019\'', '\'Stowers Institute for Medical Research\'', '\'Thanks to super-resolution microscopy, scientists have now been able to unambiguously identify physical associations between human chromosomes. The findings have brought to light a new understanding to a curious observation first made more than 50 years ago.\n\'', '\'\nThe Stowers Institute for Medical Research scientists probed these physical connections between five of the chromosomes in the human karyotype in a report recently published online in the Journal of Cell Biology.\n\"Inter-chromosome connections may prove to be an integral and pervasive governing feature of chromosome organization in many types of human cells,\" says Stowers Investigator Jennifer Gerton, Ph.D., who led the research team that investigated the basis and function of these linkages.\nThe linkages were detected during the course of research on the organization of the human genome. Tamara Potapova, Ph.D., a research specialist in the Gerton Lab, collaborated with Stowers Microscopy and Computational Biology teams to use structural image super-resolution microscopy (SIM) technology, which visualizes biological samples at nanoscale resolution, and DNA sequencing analysis in these studies.\nPotapova, first author of the paper, explains that she and her colleagues were surprised when the SIM images consistently revealed connections between five of the twenty-three human chromosomes. \"We knew there were points of contact between duplicated sister copies of chromosomes, but not between heterologous chromosomes,\" she says. \"I was fascinated by why the same five chromosomes displayed connections in many different cell types.\"\nPotapova located several previously published reports of possible inter-chromosomal linkages. Most of these observations were made during cytogenetic investigations, long before the advent of super-resolution microscopy methods.\nAn early observation of inter-chromosome linkages was published in the journal Lancet in 1961 by the British geneticist Malcolm A. Ferguson-Smith. Because of the very limited resolution of microscopy at that time, the connections were barely visible to Ferguson-Smith, now an emeritus professor at the University of Cambridge. However, in the Lancet paper, he wrote that some of the chromosomes that he observed in his cytogenetic studies seemed to be linked by their short arms like a pair of \"acrobats holding hands.\"\nThe Stowers researchers realized that the five chromosomes that displayed inter-chromosomal connections were linked together via a single shared sequence, the ribosomal DNA (rDNA). This sequence encodes the ribosomal RNA (rRNA) molecules essential to the formation of ribosomes, the protein manufacturing factories of cells. These sequences are near the ends of five different human chromosomes and can act as the \"hands\" of the acrobats, holding the different chromosomes together.\nThe researchers also detected rDNA connections in many different human cell types. rDNA links were pervasive in both healthy and diseased tissue, indicating they are not pathological, says Potapova.\nIn the paper, the Stowers researchers and their co-authors from Singapore\'s Agency for Science, Technology and Research and the Lawrence Berkeley National Laboratory propose that the structural basis of rDNA connections between chromosomes is topological interlockings, or catenations.\nThe interlocking could occur via a combination of two factors. The first factor is intense transcriptional activity in the nucleolus, the site of ribosome biogenesis in the cell nucleus. The second factor is the presence of strands of rDNA sequences from different heterologous chromosomes in the nucleolus. Because of their close proximity in the crowded environment of the nucleolus, strands of rDNA sequences can bump against each other.\nThese strands can become interlinked by the actions of the enzyme topoisomerase II. To eliminate supercoiling stress due to high levels of transcription, topoisomerase II must constantly break and rejoin DNA strands. In the paper, the researchers propose that the enzyme could entangle strands from the rDNA regions on two different chromosomes, thereby creating the connections.\nThe researchers also determined that in addition to forming rDNA connections, topoisomerase II ensures that rDNA connections between chromosomes are resolved when chromosomes divide. Besides topoisomerase II, the research team identified other factors that modulate the connections. Factors that promote the transcription of rDNA increase connections, including the c-Myc gene, a global regulator of ribosome biogenesis and protein synthesis, and the upstream binding factor (UBF) transcription factor, which coats the rDNA linkages.\nThe research findings could provide clues about the origins of the chromosomal fusions that lead to Robertsonian translocations, the most common chromosomal abnormality in humans. Robertsonian translocations are fusions between two chromosomes that contain rDNA. The proximity provided by the connections may increase the likelihood that these chromosomes end up fused together if a break occurs in the DNA. Robertsonian translocations can lead to infertility and trisomies such as Down syndrome.\nThe Gerton Lab continues to investigate whether other regions of the genome engage in inter-chromosomal connections. Gerton says \"The results from these studies have unveiled a new type of chromosome-chromosome interaction. Now we want to know if regions in addition to the rDNA can engage in these types of interaction using similar mechanisms.\"\nOther study contributors include Jay R. Unruh, Ph.D., Zulin Yu, Ph.D., and Hua Li, Ph.D., from the Stowers Institute, Giulia Rancati, Ph.D., from the Agency for Science, Technology and Research in Singapore, and Martha R. Stampfer, Ph.D., from the Lawrence Berkeley National Laboratory.\n\'', '\'Materials provided by Stowers Institute for Medical Research. Note: Content may be edited for style and length.\'', '\'\nTamara A. Potapova,  Jay R. Unruh, Zulin Yu, Giulia Rancati, Hua Li, Martha R. Stampfer, Jennifer L. Gerton. Superresolution microscopy reveals linkages between ribosomal DNA on heterologous chromosomes. Journal of Cell Biology, 2019 DOI: 10.1083/jcb.201810166\n\n\'', '\'https://www.sciencedaily.com/releases/2019/07/190703121453.htm\n\'');
INSERT INTO `scidy` VALUES (43, '\'Treatment targeted at a genetic mutation relieves psychosis symptoms\'', '\'July 3, 2019\'', '\'Elsevier\'', '\'Treatment of psychosis can be targeted to a specific genetic mutation in patients with psychotic disorders. The study provides a proof-of-principle demonstration that treatments can be tailored to a specific genotype, rather than diagnosis, to relieve symptoms. The findings also link an individual structural mutation to the underlying biology of psychosis and treatment response.\n\'', '\'\nGenetic mutations that have large effects on psychiatric disease risk are rare, with some known to occur in only one or a few families, like the mutation described in the study led by Deborah L. Levy, PhD, McLean Hospital, a psychiatric affiliate of Harvard Medical School, Cambridge, MA, USA. The mutation was a copy number variant (CNV) in which the two patients in the study had four, instead of the usual two, copies of the GLDC gene. The authors hypothesized that this mutation might reduce brain glycine, a key factor for proper glutamatergic functioning, which is disrupted in schizophrenia.\n\"The compelling aspect is that this CNV can be linked to pathophysiology, and, as the new study shows, to treatment,\" said Dr. Levy.\nThe researchers assessed whether this CNV could help guide treatment decisions by targeting the mutation to normalize its effects, a \"genotype first\" approach. \"This approach contrasts with the standard clinical practice of treating individuals on the basis of clinical symptoms or diagnosis independent of specific genetic variants,\" said Dr. Levy.\nAddition of agents to restore glutamate function, glycine or D-cycloserine, to the patients\' standard medications improved psychotic symptoms in both patients beyond their usual treatment regimens. Each of the patients also saw some reductions in other symptoms, including mood symptoms and negative symptoms of schizophrenia, including enhanced emotional engagement and less social withdrawal.\n\"It is important to note that the two subjects studied here bore little clinical resemblance, with distinctly different symptom burdens, and highly dissimilar courses of illness,\" noted first author J. Alexander Bodkin, MD, McLean Hospital. This suggests that response to the treatment arose from targeting a specific biological process, rather than clinical diagnosis per se.\n\"Most studies of rare structural variants will have very small sample sizes, complicating the usual approach to statistical analysis. Nevertheless, because the effects of a targeted treatment can be large, it is important to prioritize opportunities to study even small groups of patients who may benefit,\" observed author Charity J. Morgan, University of Alabama, Birmingham, AL, USA.\n\"Psychiatry is in the very early days of precision medicine, i.e., the effort to match particular patients to the specific treatments that they need. In their article, Dr. Levy and her colleagues provide a wonderful example of this approach,\" said John Krystal, MD, Editor of Biological Psychiatry. \"The substances that they administered, glycine and D-cycloserine, do not produce noticeable behavioral effects in healthy people or in patients with psychotic disorders. However, because these substances replaced a deficient co-factor involved in neural communication in these particular individuals, their administration alleviated mood and psychosis symptoms. As in these cases, we expect psychiatry to develop more instances where specific treatments can be developed to meet the needs of particular groups of patients.\"\n\'', '\'Materials provided by Elsevier. Note: Content may be edited for style and length.\'', '\'\nJ. Alexander Bodkin, Michael J. Coleman, Laura J. Godfrey, Claudia M.B. Carvalho, Charity J. Morgan, Raymond F. Suckow, Thea Anderson, Dost Ongur, Marc J. Kaufman, Kathryn E. Lewandowski, Arthur J. Siegel, Elliot Waldstreicher, Christopher M. Grochowski, Daniel C. Javitt, Dan Rujescu, Scott Hebbring, Richard Weinshilboum, Stephanie Burgos Rodriguez, Colette Kirchhoff, Timothy Visscher, Alexander Vuckovic, Allison Fialkowski, Shane McCarthy, Dheeraj Malhotra, Jonathan Sebat, Donald C. Goff, James I. Hudson, James R. Lupski, Joseph T. Coyle, Uwe Rudolph, Deborah L. Levy. Targeted Treatment of Individuals With Psychosis Carrying a Copy Number Variant Containing a Genomic Triplication of the Glycine Decarboxylase Gene. Biological Psychiatry, 2019; DOI: 10.1016/j.biopsych.2019.04.031\n\n\'', '\'https://www.sciencedaily.com/releases/2019/07/190703121415.htm\n\'');
INSERT INTO `scidy` VALUES (44, '\'Blood pressure drug linked with increased risk of bowel condition\'', '\'July 3, 2019\'', '\'Imperial College London\'', '\'A type of blood pressure lowering medication, called a calcium-channel blocker, may be linked with an increased risk of a type of bowel condition called diverticulosis.\n\'', '\'\nThe new early-stage research finding comes from a team of scientists led by Imperial College London, who investigated the effectiveness and side effects of three common blood pressure medications: ACE-inhibitors, beta-blockers and calcium channel blockers.\nHigh blood pressure affects one in ten adults across the globe, and increases the risk of heart attack and stroke. The most common treatments for high blood pressure are lifestyle changes and medications.\nHowever, despite the three main medications being taken by millions, investigating their potential side effects (as well as studying their effectiveness for treating other diseases), can be difficult and often involves lengthy and expensive clinical trials.\nTo overcome this problem, the research team, led by Imperial\'s School of Public Health, used genetic analyses to study the effects of the drugs.\nBy investigating versions of genes that mimic the effects of these drugs, the team were able to study the drugs\' effectiveness -- and their potential side effects.\nFirst, the researchers, who published their work in the journal Circulation, identified the proteins targeted by the drugs, and which help lower blood pressure. Next, they analysed genetic data from around 750,000 people and identified the so-called genetic variants that code for these proteins.\nThe team, who included researchers from LMU Munich, then studied whether these gene variants -- which cause increased production of these proteins -- were linked to an increased or decreased risk of other diseases.\nThe good news was that, as expected, these so-called genetic variants (which coded for proteins involved in lowering blood pressure) were linked to lower heart disease and stroke risk.\nHowever after assessing the risk of around 900 different diseases -- using data from the UK Biobank study -- the team found that the versions of genes related to the effects of a particular type of calcium channel blocker -- the non-dihydropyridine class, were linked to an increased the risk of a bowel condition called diverticulosis.\nThe team compared their findings with further genetic data, and supported the potential link with an increased risk of the bowel condition.\nThe link now needs further investigation with larger trials, explains Dr Dipender Gill, co-lead author of the research from Imperial\'s School of Public Health: \"This is the first time that this class of blood pressure drug has been associated with diverticulosis. We\'re not sure of the underlying mechanism -- although it may relate to effects on the function of intestine muscles, which perform contractions to transport food through the gut.\"\nDr Joanna Tzoulaki, senior author from Imperial\'s School of Public Health added: \"The study of genetic variants that mimic the effect of drugs is evolving as a powerful concept to help prioritise clinical trials and design clinical trials more likely to be successful.\"\nDr Gill cautions the findings should not change current prescribing guidelines and that people should not stop taking their medication unless first consulting their doctor.\nHe added: \"These findings should not change clinical practice, but instead should act as a catalyst for further research.\"\n\'', '\'Materials provided by Imperial College London. Original written by Kate Wighton. Note: Content may be edited for style and length.\'', 'NULL', '\'https://www.sciencedaily.com/releases/2019/07/190703121413.htm\n\'');
INSERT INTO `scidy` VALUES (45, '\'Perfect timing: Making the \'switch\' from juvenile to adult\'', '\'July 3, 2019\'', '\'University of Rochester Medical Center\'', '\'Very little is known about how the onset of puberty is controlled in humans, but the discovery of a new gene in the roundworm C. elegans could be the \'missing link\' that determines when it\'s time to make this juvenile-to-adult transition.\n\'', '\'\nThe more obvious signs of the transition of juvenile-to-adult tend to be external -- body morphology, matured genitalia -- but nervous system changes are also happening at the same time. In humans, the maturation of the brain during adolescence is associated with increased vulnerability to a variety of neuropsychiatric disorders, so a better understanding of these processes is important for understanding mental health as well as basic neurobiology.\nTwo new studies in the labs of Douglas Portman, Ph.D. at the University of Rochester Medical Center and David Fitch at New York University, published in Developmental Cell and eLife, identified a new developmental timing mechanism involving a long non-coding RNA in the microscopic roundworm C. elegans. Their research revealed a surprising new molecular mechanism that controls the timing of sex-specific changes in body shape, the maturation of neural circuits, and behavior.\nC. elegans has long been used by researchers to understand fundamental mechanisms in biology. Many of the discoveries made using these worms apply throughout the animal kingdom and this research has led to a broader understanding of human biology. In fact, three Nobel Prizes in medicine and chemistry have been awarded for discoveries involving C. elegans.\nThe researchers identified a new gene that, when disrupted, delays the transition from the juvenile to the adult stage. Surprisingly, this gene, called lep-5, does not act as a protein, as most genes do. Instead, it functions as a long non-coding RNA (lncRNA), a recently discovered class of genes whose functions remain largely mysterious. The team observed that this lncRNA is important for promoting the juvenile-to-adult transition by directly interacting with LIN-28 and LEP-2, a C. elegans gene similar to MKRN3. Because the human versions of LEP-2 and LIN-28 are both involved in the timing of puberty, the new research suggests that a yet-to-be-discovered lncRNA might be essential to this process in humans as well.\nIn the roundworm nervous system, some neural circuits undergo a functional transition in males as they become sexually mature adults, which is critical for generating adult-specific behaviors important for reproductive success. The male tail also undergoes a change in shape that enables mating behavior. The researchers found that this same pathway controls both the functional maturation of these circuits and the shape of the tail. Roundworms carrying mutations in lep-5 become physically mature adults, but their nervous system remains arrested in the juvenile stage, and their tails retain a juvenile form.\nWith respect to changes in behavior, the pathway regulates this timing by acting in the nervous system itself, not in a tissue that sends timing signals to the nervous system. Moreover, individual neurons manage their own developmental clocks. A timed \"pulse\" of lep-5 activity during the juvenile stage causes LIN-28 to become inactive, allowing the transition to adulthood to proceed.\nContinued studies of the mechanisms identified in these studies will help scientists better understand the ways in which genetic and environmental cues regulate the transition to adulthood in humans. This research was supported by the National Institute of General Medical Sciences and National Science Foundation grants to Portman and Fitch.\n\'', '\'Materials provided by University of Rochester Medical Center. Note: Content may be edited for style and length.\'', '\'\nHannah Lawson, Edward Vuong, Renee M Miller, Karin Kiontke, David HA Fitch, Douglas S Portman. The Makorin lep-2 and the lncRNA lep-5 regulate lin-28 to schedule sexual maturation of the C. elegans nervous system. eLife, 2019; 8 DOI: 10.7554/eLife.43660\n\n\'', '\'https://www.sciencedaily.com/releases/2019/07/190703121359.htm\n\'');
INSERT INTO `scidy` VALUES (46, '\'Quorn protein builds muscle better than milk protein\'', '\'July 3, 2019\'', '\'University of Exeter\'', '\'A study has found that mycoprotein, the protein-rich food source that is unique to Quorn products, stimulates post-exercise muscle building to a greater extent than milk protein.\n\'', '\'\nThe study evaluated the digestion of protein, which allows amino acids (the building blocks of protein) to increase in the bloodstream and then become available for muscle protein building in 20 healthy, trained young men at rest and following a bout of strenuous resistance exercise.\nThe young men performed the exercise and were then given either milk protein or mycoprotein.\nTheir muscle building rates were then measured using stable isotope labelled \"tracers\" in the hours following protein consumption.\nAnimal proteins like milk are an excellent source for muscle growth, so they provide a useful comparison for testing other protein sources.\nThe results showed that while those who ingested milk6 protein increased their muscle building rates by up to 60%, those who had mycoprotein increased their muscle growth rates (MGRs) by more than double this -- showing that mycoprotein, the main ingredient in all Quorn products, is a more effective source of protein to promote muscle growth.\n\"These results are very encouraging when we consider the desire of some individuals to choose non-animal derived sources of protein to support muscle mass maintenance or adaptations with training,\" said Dr Benjamin Wall, Associate Professor of Nutritional Physiology, University of Exeter.\n\"Our data show that mycoprotein can stimulate muscles to grow faster in the hours following exercise compared with a typical animal comparator protein (milk protein) -- we look forward to seeing whether these mechanistic findings translate to longer term training studies in various populations.\"\nTim Finnigan, Chief Scientific Adviser for Quorn Foods, said \"We\'re excited to see this data being presented by the University of Exeter at ECSS. In a world where many people are trying to cut back on their meat consumption, either for environmental or health reasons, we\'re happy to be able to offer an alternative protein that can provide exceptional nutrition and muscle growth, all while being meat-free.\"\nRecent research has suggested that current recommendations for protein intake are too low -- some scientists have calculated that minimum protein requirements could have been underestimated by as much as 30-50% in some populations.1\nThe British Nutrition Foundation already recommends mycoprotein as a good source of dietary protein, both for everyday life and for sport and exercise.\nHowever, in the UK roughly a third of total protein consumption comes from meat products -- and increasing meat intake may have serious consequences for public health and for the environment.\nA pivot to \"alternative\" sources of protein therefore may be advisable -- and mycoprotein is well placed to fill the gap.\n\'', '\'Materials provided by University of Exeter. Note: Content may be edited for style and length.\'', 'NULL', '\'https://www.sciencedaily.com/releases/2019/07/190703121431.htm\n\'');
INSERT INTO `scidy` VALUES (47, '\'Obese people outnumber smokers two to one\'', '\'July 2, 2019\'', '\'Cancer Research UK\'', '\'New figures show that people who are obese now outnumber people who smoke two to one in the UK, and excess weight causes more cases of certain cancers than smoking, as the charity urges government action to tackle obesity.\n\'', '\'\nAlmost a third of UK adults are obese** and, while smoking is still the nation\'s biggest preventable cause of cancer and carries a much higher risk of the disease than obesity, Cancer Research UK\'s analysis revealed that being overweight or obese trumps smoking as the leading cause of four different types of cancer***.\nExcess weight causes around 1,900 more cases of bowel cancer than smoking in the UK each year. The same worrying pattern is true of cancer in the kidneys (1,400 more cases caused by excess weight than by smoking each year in the UK), ovaries (460) and liver (180).\nCancer Research UK launched a nationwide campaign this week to increase awareness of the link between obesity and cancer. Extra body fat sends out signals that can tell cells to divide more often and can cause damage that builds up over time and raises the risk of cancer.\nThe campaign compares smoking and obesity to show how policy change can help people form healthier habits, not to compare tobacco with food.\nMichelle Mitchell, Cancer Research UK\'s chief executive, said: \"As smoking rates fall and obesity rates rise, we can clearly see the impact on a national health crisis when the Government puts policies in place -- and when it puts its head in the sand.\n\"Our children could be a smoke-free generation, but we\'ve hit a devastating record high for childhood obesity, and now we need urgent Government intervention to end the epidemic. They still have a chance to save lives.\n\"Scientists have so far identified that obesity causes 13 types of cancer but the mechanisms aren\'t fully understood. So further research is needed to find out more about the ways extra body fat can lead to cancer.\"\nThe charity wants the Government to act on its ambition to halve childhood obesity rates by 2030 and introduce a 9pm watershed for junk food adverts on TV and online, alongside other measures such as restricting promotional offers on unhealthy food and drinks.\nProfessor Linda Bauld, Cancer Research UK\'s prevention expert, commented: \"There isn\'t a silver bullet to reduce obesity, but the huge fall in smoking over the years -- partly thanks to advertising and environmental bans -- shows that Government-led change works. It was needed to tackle sky-high smoking rates, and now the same is true for obesity.\n\"The world we live in doesn\'t make it easy to be healthy and we need Government action to fix that, but people can also make changes themselves; small things like swapping junk food for healthier options and keeping active can all add up to help reduce cancer risk.\"\nNotes\n* In the UK there are around 13.4 million non-smoking adults who are obese (body mass index 30+), 6.3 million adult smokers who are not obese, and 1.5 million adults who smoke and are obese -- so among UK adults, people who are obese outnumber people who smoke 2:1, based on calculations by the Cancer Intelligence Team at Cancer Research UK\n** There are around 14.9 million obese adults in the UK, which is roughly 29% of the adult UK population -- the Cancer Intelligence Team at Cancer Research UK calculated this by combining adult (18+) population estimates for 2017 from Office for National Statistics with adult (16+) obesity prevalence data from Health Survey for England 2017, Scottish Health Survey 2017, National Survey for Wales 2017 and Health Survey Northern Ireland 2017\n*** Brown, Rumgay et al, 2018: The fraction of cancer attributable to modifiable risk factors in England, Wales, Scotland, Northern Ireland, and the United Kingdom in 2015 (with overweight defined as body mass index 25+ and obese defined as body mass index 30+)\n\'', '\'Materials provided by Cancer Research UK. Note: Content may be edited for style and length.\'', 'NULL', '\'https://www.sciencedaily.com/releases/2019/07/190702211335.htm\n\'');
INSERT INTO `scidy` VALUES (48, '\'Tiny change has big effects, reverses prediabetes in mice\'', '\'July 4, 2019\'', '\'University of Utah Health\'', '\'A small chemical change -- shifting the position of two hydrogen atoms -- makes the difference between mice that are healthy or that have insulin resistance and fatty liver, major risk factors for diabetes and heart disease. Making the change prevented the onset of these symptoms in mice fed a high-fat diet and reversed these prediabetes obese mice. Published in Science, the finding pinpoints a \'druggable\' target that could be used to develop therapies for diabetes.\n\'', '\'\nThe scientists changed the trajectory of metabolic disease by deactivating an enzyme called dihydroceramide desaturase 1 (DES1). Doing so stopped the enzyme from removing the final hydrogens from a fatty lipid called ceramide, having an effect of lowering the total amount of ceramides in the body.\nThe finding highlights a role for ceramides in metabolic health and pinpoints DES1 as a \"druggable\" target that could be used to develop new therapies for metabolic disorders such as prediabetes, diabetes and heart disease -- that affect the health of hundreds of millions of Americans. Scientists at University of Utah Health and Merck Research Laboratories led the research, published online in Science on July 4, 2019.\n\"We have identified a potential therapeutic strategy that is remarkably effective, and underscores how complex biological systems can be deeply affected by a subtle change in chemistry,\" says Scott Summers, Ph.D., chair of Nutrition and Integrative Physiology at U of U Health, who was co-senior author on the study with David Kelley, M.D., formerly of Merck Research Laboratories.\n\"Our work shows that ceramides have an influential role in metabolic health,\" says Summers. \"We\'re thinking of ceramides as the next cholesterol.\"\nThis isn\'t the first time that Summers\' group has found that lowering ceramides could reverse signs of diabetes and metabolic disease. However, techniques used in previous experiments caused severe side effects, showing the approach would not be suitable for therapeutic applications.\nThis time, rather than taking a sledgehammer to the problem, they developed a fine scalpel. They wondered whether making the smallest change possible and at a precise time and place might yield better results.\nTo lower ceramides, the investigators blocked the final step of ceramide synthesis in two ways. Summers\' group genetically engineered mice in which the gene coding for DES1 could be switched off during adulthood and deactivated the gene from tissues throughout the body, or alternatively from either liver or fat cells. Kelley\'s group injected short hairpin RNA into the adult liver, a method that selectively lowered production of DES1 by destroying the RNA precursor.\nThe scientists tested the new approaches first by placing adult mice on a high-fat diet -- one that resembled cookie dough with plenty of sugar and six times the fat of a normal rodent diet. The mice gained two times their body weight within three months. Along with obesity came a strain on their metabolic health. They developed insulin resistance and fat accumulated in the liver, both signs of metabolic disease.\nWithin weeks after lowering ceramides using either technique, there were significant changes. Mice remained obese but their metabolic health improved. Fat cleared from the liver and they responded to both insulin and glucose like a healthy, skinny mouse. In contrast to previous interventions, mice remained healthy during the two-month investigation. Long-term effects on health are currently under investigation.\n\"Their weight didn\'t change but the way they handled nutrients did,\" says Summers. \"The mice were fat but they were happy and healthy.\"\nIn another paradigm, lowering ceramides before putting the mice on a high-fat diet prevented weight gain and insulin resistance.\nAlthough the impact of lowering ceramides in humans is still unknown, there is evidence that ceramides are linked to metabolic disease, says Summers. He points out that clinics are already performing ceramide screening tests to gauge an individual\'s risk for developing heart disease.\nSummers and Kelley are now developing drugs that inhibit DES1 with a goal of making new therapeutics. \"This project provides substantial validation that this is a discreet and highly effective point of intervention,\" says Kelley.\nWhen the Good Goes Bad\nIf ceramides cause poor health, why do we have them in the first place? Summers\' group addressed the question by measuring how the lipid affects metabolism. They found that ceramides trigger a number of mechanisms that promote the storage of fat in cells. They also impair cells\' ability to use glucose, a type of sugar, as fuel.\nThe evidence for these effects includes activation of a molecular pathway, Akt/PKB, that inhibits both the ability of cells to synthesize sugars and to take them up from the bloodstream. At the same time, ceramides slow the turnover of fatty acids in part by causing cells in the liver to increase fatty acid storage and adipose tissue to burn less fat.\nThe shift in how cells use fuel is an advantage in the short-term, says Summers. This is because ceramides have another role in stiffening the cell membrane. Further, promoting fat storage increases production of ceramides. These data lead to a model suggesting that one benefit of ceramides is that they protect the cell. When food is plentiful and cells store lots of fat, the increase in ceramide levels strengthen the cells\' outer membrane, preventing ruptures.\n\"Serving in this role is usually good but it can potentially be bad,\" explains Trevor Tippetts, a graduate student in Summers\' lab. He, U of U Health research assistant professor Bhagirath Chaurasia, Ph.D., and two of their Merck colleagues, Rafael Mayoral Moñibas, Ph.D., and Jinqi Liu, Ph.D., share lead authorship.\nTippetts explains that problems arise in times of chronic overabundance, such as during obesity, when there are persistently high levels of ceramides. Summers\' team speculate that sustained impairment of metabolic homeostasis leads to insulin resistance and fatty liver disease.\nThe results hint at ceramide\'s normal role. \"We think that ceramides evolved to become a nutritional sensor,\" says Chaurasia. He says that ceramides serve as a signal, helping the body to cope when the amount of fat that is coming into cells is exceeding its energetic needs, and its storage capacity.\nThese findings are leading to a deep understanding of how cells in the body assess nutrient status and adapt accordingly. \"To me, that\'s the really exciting result,\" Chaurasia says.\n\'', '\'Materials provided by University of Utah Health. Note: Content may be edited for style and length.\'', '\'\nBhagirath Chaurasia, Trevor S. Tippetts, Rafael Mayoral Monibas, Jinqi Liu, Ying Li, Liping Wang, Joseph L. Wilkerson, C. Rufus Sweeney, Renato Felipe Pereira, Doris Hissako Sumida, J. Alan Maschek, James E. Cox, Vincent Kaddai, Graeme Iain Lancaster, Monowarul Mobin Siddique, Annelise Poss, Mackenzie Pearson, Santhosh Satapati, Heather Zhou, David G. Mclaren, Stephen F. Previs, Ying Chen, Ying Qian, Aleksandr Petrov, Margaret Wu, Xiaolan Shen, Jun Yao, Christian N. Nunes, Andrew D. Howard, Liangsu Wang, Mark D. Erion, Jared Rutter, William L. Holland, David E. Kelley, Scott A. Summers. Targeting a ceramide double bond improves insulin resistance and hepatic steatosis. Science, 2019 DOI: 10.1126/science.aav3722\n\n\'', '\'https://www.sciencedaily.com/releases/2019/07/190704191347.htm\n\'');
INSERT INTO `scidy` VALUES (49, '\'After concussion, biomarkers in the blood may help predict recovery time\'', '\'July 3, 2019\'', '\'American Academy of Neurology\'', '\'A study of high school and college football players suggests that biomarkers in the blood may have potential use in identifying which players are more likely to need a longer recovery time after concussion.\n\'', '\'\n\"With so many people sustaining concussions and a sizeable number of them having prolonged symptoms and recovery, any tools we can develop to help determine who would be at greater risk of problems would be very beneficial, so these results are a crucial first step,\" said study author Timothy B. Meier, PhD, of the Medical College of Wisconsin in Milwaukee and a member of the American Academy of Neurology.\nThe study involved 41 high school and college football players who experienced a concussion during the season. None of the players lost consciousness with their concussions. The players were matched with 43 football players of the same level, age and position who did not have a concussion during that season.\nAll of the participants had blood tests at the beginning of the season. Those who had concussions had blood tests within six hours after the injury, then again 24 to 48 hours later and also eight, 15 and 45 days later. Those who did not have concussions had tests at similar times for comparison.\nThe tests looked at levels of seven biomarkers for inflammation that have been related to more severe brain injury. Of the seven biomarkers, two were elevated for those with concussion at six hours after the injury compared to the athletes with no concussion. The biomarkers interleukin 6 and interleukin 1 receptor antagonist were both elevated at six hours after concussion.\nFor interleukin 6, levels at the beginning of the study were 0.44 picograms per milliliter (pg/mL) for those who later had concussions and 0.40 pg/mL for those who did not have concussions. At six hours after the injury, those with concussions had levels of 1.01 pg/mL, compared to levels of 0.39 at a similar time for those without concussions.\n\"These results demonstrate a meaningful increase in the levels of interleukin 6 for athletes who sustained a concussion compared to athletes who did not,\" said Meier.\nAthletes with higher levels of interleukin 6 six hours after the injury were also more likely to take longer to recover from their symptoms. Overall, the athletes with concussions had symptoms for an average of 8.9 days. Eight of the 17 athletes with concussion and high interleukin 6 levels at six hours after injury, compared to their levels at the beginning of the season, still had concussion symptoms eight days after the injury.\n\"Eventually, these results may help us better understand the relationship between injury and inflammation and potentially lead to new treatments,\" Meier said.\n\'', '\'Materials provided by American Academy of Neurology. Note: Content may be edited for style and length.\'', '\'\nMorgan E. Nitta, Jonathan Savitz, Lindsay D. Nelson, T. Kent Teague, James B. Hoelzle, Michael A. McCrea, Timothy B. Meier. Acute elevation of serum inflammatory markers predicts symptom recovery after concussion. Neurology, 2019; 10.1212/WNL.0000000000007864 DOI: 10.1212/WNL.0000000000007864\n\n\'', '\'https://www.sciencedaily.com/releases/2019/07/190703171853.htm\n\'');
INSERT INTO `scidy` VALUES (50, '\'Protein-linked sugars are crucial for the uptake of proteins linked to Parkinson\'s disease\'', '\'July 3, 2019\'', '\'University of Pennsylvania\'', '\'New research shows how glycoproteins, proteins with added sugar molecules, influence the uptake of protein aggregates that are associated with Parkinson\'s disease. The researchers also identified a specific presynaptic protein as a key regulator in this process, which opens the door for future research into new therapeutic targets.\n\'', '\'\nA new study from Elizabeth Rhoades and postdoc Melissa Birol found that when alpha-synuclein binds to extracellular glycoproteins, proteins with added sugar molecules, it can be taken up by neurons more easily. The paper also identified a specific presynaptic protein, neurexin 1?, as a key regulator in this process and a potential therapeutic target. Their findings were published in the journal PLOS Biology.\nIn one possible model for the pathology of Parkinson\'s disease, bundles of alpha-synuclein proteins, known as aggregates, form inside a neuron. This then leads to cell death and the release of alpha-synuclein protein clusters that are taken up by other neurons. Since neurodegenerative diseases have typical progression patterns, knowing how alpha-synuclein moves between neurons in the brain helps researchers understand disease propagation.\nPrevious work from the Rhoades lab implicated the presence of a glycan binding site on alpha-synuclein. This finding, combined with Birol\'s experience in analyzing protein-membrane interactions, led to this study of how alpha-synuclein interacts with cell membranes.\nBirol was able to enzymatically remove specific glycans from the cell surface to see how their presence or absence would change how alpha-synuclein was taken up by neurons. The study found that when glycans were removed, the amount of alpha-synuclein clusters taken up by cells was greatly reduced.\nAnd by analyzing giant plasma membrane vesicles, synthetic membranes derived from components of real cells that have the same protein and lipid composition, Birol was also able to see the detailed physical interactions between alpha-synuclein and glycans. \"There\'s a structural basis for the alpha-synuclein binding to the glycan, and when the glycans are removed, it changes the nature of the interaction of alpha-synuclein with the cell membrane,\" explains Rhoades.\nThis research focused on the acetylated form of alpha-synuclein proteins, which is present in both healthy and diseased neurons and is less frequently studied. They found that the acetylated form was more effective at forming clusters of proteins inside neurons and was required for interactions with glycans. \"No one\'s really stressed the importance of these acetylated versions,\" Birol says. \"Generally, we need take a step back in trying to understand how this protein may be propagating between cells, and I think glycans could be an aspect.\"\nRhoades and Birol say that the most unexpected finding was the discovery of neurexin 1? as a potential partner in how alpha-synuclein is taken up by neurons. They hope that future research on this presynaptic protein could provide insights into new treatment strategies for Parkinson\'s and other neurodegenerative diseases.\nIn the near term, Rhoades and her group hope to obtain higher-resolution structural information of alpha-synuclein proteins bound to glycans. They also hope that this study will inspire future research on alpha-synuclein acetylation and the role of glycans in the progression of the disease and will provide an impetus to look at previously unstudied protein modifications that might be connected to Parkinson\'s disease.\n\"Some cells spontaneously internalize these [alpha-synuclein] proteins and some do not. It has generally been assumed that there are alpha-synuclein specific receptors on the cells that do internalize aggregates. That may or may not be true, but [our study] suggests that it\'s not just the protein receptors but the glycans that are also important,\" says Rhoades.\nThis research was supported by the Michael J. Fox Foundation for Parkinson\'s Research.\n\'', '\'Materials provided by University of Pennsylvania. Note: Content may be edited for style and length.\'', '\'\nMelissa Birol, Slawomir P. Wojcik, Andrew D. Miranker, Elizabeth Rhoades. Identification of N-linked glycans as specific mediators of neuronal uptake of acetylated α-Synuclein. PLOS Biology, 2019; 17 (6): e3000318 DOI: 10.1371/journal.pbio.3000318\n\n\'', '\'https://www.sciencedaily.com/releases/2019/07/190703150522.htm\n\'');
INSERT INTO `scidy` VALUES (51, '\'How protein mutation is involved in rare brain development disorder\'', '\'July 3, 2019\'', '\'McGill University\'', '\'Christianson Syndrome is a rare disorder whose symptoms include intellectual disability, seizures and difficulty standing or walking. Researchers focusing on the intellectual disability aspect of the disease, have shown for the first time how a specific mutant form of the SLC9A6 encoding gene for the NHE6 protein affects the ability of neurons to form and strengthen connections.\n\'', '\'\nNow, researchers at McGill University focusing on the intellectual disability aspect of the disease, have shown for the first time how a specific mutant form of the SLC9A6 encoding gene for the NHE6 protein affects the ability of neurons to form and strengthen connections. The findings, which the researchers hope could eventually lead to new treatments for patients, are published online in the journal Neurobiology of Disease.\n\"NHE6 functions like a GPS inside of brain cells, helping other proteins navigate to the correct location to allow the neurons to function properly and remodel the connections they form between themselves during learning and memory situations,\" explains Dr. Anne McKinney, Professor in the Department of Pharmacology and Therapeutics at McGill\'s Faculty of Medicine and the study\'s senior author. \"This protein regulates pH of the vesicles, which contain the cargo that moves inside the brain cell. It prevents it from becoming too acidic or too alkali. We now show that if this protein loses its function because of a mutation, then other proteins can no longer be sent to the right places, and thus these neurons are unable to properly undergo learning-type mechanisms. Using methods to regulate the pH of the vesicles we can rescue the cargo trafficking and learning of the neuron.\"\nUsing mouse models to study the hippocampus\nTo make their discovery, the researchers grew mouse neurons on a dish, expressing a mutant version of SLC9A6 discovered in patients. Using high-resolution microscopy and electrophysiology they examined changes in appearance of these brain cells as well as how they responded to artificial learning and memory-type stimulations in a dish.\n\"We found that by attempting to rescue the \'GPS\' function of the protein by compensating with other pharmacological agents, we were able to restore at least some of the proper mechanisms to allow other proteins to be trafficked around the cell normally and thus restore their ability to \'learn\',\" notes Andy Gao a PhD student in Dr. McKinney\'s lab and the study\'s first author.\nA hope for potential therapies\nThe first study to clearly demonstrate that mutations in SLC9A6 can lead to changes in synaptic function that could be related to the cognitive deficits associated with Christianson Syndrome, the researchers hope that these insights will eventually provide more clues as to how to modify the impact of the mutation in order to provide clinical benefit.\n\"Interestingly enough, other groups are starting to show that the implicated protein is actually expressed less as well in other more common neurodegenerative disorders, such as Parkinson\'s and Alzheimer\'s Diseases,\" notes Dr. McKinney, who is also Associate Dean, Academic Affairs at the Faculty of Medicine. \"Through our work, we can start to develop potential therapeutic targets to improve the quality of life, not only for those suffering from Christianson Syndrome, but from other disorders as well where NHE6 is perturbed.\"\n\'', '\'Materials provided by McGill University. Note: Content may be edited for style and length.\'', '\'\nAndy Y.L. Gao, Alina Ilie, Philip K.Y. Chang, John Orlowski, R. Anne McKinney. A Christianson syndrome-linked deletion mutation (Δ287ES288) in SLC9A6 impairs hippocampal neuronal plasticity. Neurobiology of Disease, 2019; 130: 104490 DOI: 10.1016/j.nbd.2019.104490\n\n\'', '\'https://www.sciencedaily.com/releases/2019/07/190703150520.htm\n\'');
INSERT INTO `scidy` VALUES (52, '\'Ovarian and breast cancer research finds new ways BRCA1 gene functions\'', '\'July 3, 2019\'', '\'University of Birmingham\'', '\'Research has found important new ways that the BRCA1 gene functions which could help develop our understanding of the development of ovarian and breast cancers.\n\'', '\'\nThe research, published in Nature today (July 3rd), was led by experts at the University of Birmingham\'s Birmingham Centre for Genome Biology and Institute of Cancer and Genomic Sciences and is part of a five-year research project which is playing a pivotal role in identifying and understanding breast cancer genes.\nFirst author Manolo Daza-Martin, of the University of Birmingham, explained: \"No two people are born the same and, as a result, we all have slightly different chances of developing diseases during our lifetimes -- this is the result of natural variation in our genes.\n\"On top of this natural variation, about one in a thousand people inherit from one of their parents a damaged, or \'mutated\', copy of a gene called BRCA1.\n\"Previous research has shown us that in cells the BRCA1 gene makes a protein that helps repair damage to broken DNA. Therefore, people who inherit a faulty BRCA1 gene are less able to repair damage that inevitably accumulates in their DNA over time -- putting them at higher risk of ovarian and breast cancer.\nHollywood actress Angelina Jolie had a double mastectomy and announced she was to have her ovaries removed in 2013 after being tested positive for the BRCA1 genetic mutation. Her mother died at the young age of 56 due to cancer.\nDNA damage can also occur when cells have difficulties copying their DNA leaving it vulnerable to breakage. BRCA1 helps protect DNA when the copying machinery gets stuck, but it was not known how. Now University of Birmingham researchers, in collaboration with scientists at Imperial College London, have found that BRCA1 changes shape in order to protect vulnerable DNA until the copying machinery can be restarted. In addition, the researchers found that in some patients with a personal or family history of breast and ovarian cancer, the protective role of BRCA1 in DNA-copying is disabled -- while its break repair function is still active.\nJoint corresponding author Dr Ruth Densham, of the University of Birmingham\'s Institute of Cancer and Genomic Sciences, added: \"BRCA1 is like a DNA Damage Scene Coordinator, whose role is to coordinate emergency response units at a damage site in order to help repair. It was surprising to find out that BRCA1 changes shape depending on the type of damage it finds at the scene, and this shape change alters the way the cell responds.\"\nLead and corresponding author Professor Jo Morris, also of the University of Birmingham\'s Institute of Cancer and Genomic Sciences, said: \"Our research could be important for understanding how cancers develop and means we could have identified a new way of supressing tumours.\n\"We are long way from it, but ultimately this may alter how cancer patients are treated. We will now continue this important research into the role of BRCA1\'s DNA copying function in cancer development.\"\nThe average woman in the UK has a 12.5 per cent chance of developing breast cancer at some point in her life.\nAbout one in 20 (five per cent) of the 50,000 women diagnosed with breast cancer every year carries an inherited gene fault like BRCA1.\nA female BRCA1 carrier has between a 60 and 90 per cent chance of developing breast cancer, and around a 40 to 60 per cent chance of ovarian cancer. The precise figure for an individual woman will vary according to several things, such as her age, the number of affected family members, and the exact nature of the fault in the gene.\n\'', '\'Materials provided by University of Birmingham. Note: Content may be edited for style and length.\'', '\'\nManuel Daza-Martin, Katarzyna Starowicz, Mohammed Jamshad, Stephanie Tye, George E. Ronson, Hannah L. MacKay, Anoop Singh Chauhan, Alexandra K. Walker, Helen R. Stone, James F. J. Beesley, Jennifer L. Coles, Alexander J. Garvin, Grant S. Stewart, Thomas J. McCorvie, Xiaodong Zhang, Ruth M. Densham, Joanna R. Morris. Isomerization of BRCA1–BARD1 promotes replication fork protection. Nature, 2019; DOI: 10.1038/s41586-019-1363-4\n\n\'', '\'https://www.sciencedaily.com/releases/2019/07/190703134058.htm\n\'');