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  • richardmitnick 1:58 pm on March 17, 2014 Permalink | Reply
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    From Berkeley Lab: “Vast Gene-Expression Map Yields Neurological and Environmental Stress Insights” 


    Berkeley Lab

    March 16, 2014
    Dan Krotz 510-486-4019 dakrotz@lbl.gov

    A consortium led by scientists from the U.S. Department of Energy’s Lawrence Berkeley National Laboratory (Berkeley Lab) has conducted the largest survey yet of how information encoded in an animal genome is processed in different organs, stages of development, and environmental conditions. Their findings paint a new picture of how genes function in the nervous system and in response to environmental stress.

    They report their research this week in the Advance Online Publication of the journal Nature.

    The scientists studied the fruit fly, an important model organism in genetics research. Seventy percent of known human disease genes have closely related genes in the fly, yet the fly genome is one-thirtieth the size of ours. Previous fruit fly research has provided insights on cancer, birth defects, addictive behavior, and neurological diseases. It has also advanced our understanding of processes common to all animals such as body patterning and synaptic transmission.

    fly
    The remarkable complexity of the fruit fly transcriptome comes to life in this fruit fly embryo. Blue dye indicates the presence of RNA molecules in the brain from a previously uncharacterized gene (CG42748) that encodes hundreds of different proteins. No image credit.

    In the latest scientific fruit from the fruit fly, the consortium, led by Susan Celniker of Berkeley Lab’s Life Sciences Division, generated the most comprehensive map of gene expression in any animal to date. Scientists from the University of California at Berkeley, Indiana University at Bloomington, the University of Connecticut Health Center, and several other institutions contributed to the research.

    In all organisms, the information encoded in genomes is transcribed into RNA molecules that are either translated into proteins, or utilized to perform functions in the cell. The collection of RNA molecules expressed in a cell is known as its transcriptome, which can be thought of as the “read out” of the genome.

    While the genome is essentially the same in every cell in our bodies, the transcriptome is different in each cell type and constantly changing. Cells in cardiac tissue are radically different from those in the gut or the brain, for example.

    The transcriptome also changes rapidly in response to environmental challenges. These dynamics in gene expression allow our bodies to adapt to changes such as temperature or exposure to chemicals.

    graph
    The broad range of genes that respond to environmental stress is evident in this genome-wide map of genes that are up or down-regulated when fruit flies are exposed to the heavy metal cadmium. Labeled genes are those that showed a 20-fold change in response. No image credit.

    To map the transcriptome, the scientists used deep sequencing technology to generate 1.2 trillion bases of RNA sequence data. They analyzed RNA in 29 fruit fly tissue types, 25 cell lines, and “environmental challenge” scenarios including heat, cold, heavy metal poisoning, and acute exposure to pesticides.

    The combination of extremely deep sequencing and a diverse array of tissues and conditions resulted in a full-body map of RNA activity, which revealed new genes and rare RNAs that are expressed in only one tissue type. Among the discoveries are the unexpected complexity and diversity of the RNAs present in tissues of the nervous system, and previously unknown genes implicated in stress response.

    In samples of the fly’s nervous system, the scientists found about 100 genes that can encode hundreds or even thousands of different types of proteins. Many of these proteins are made in the developing embryo during the early formation of the nervous system. This hints at a previously unknown source of the complexity of the brain, given that most genes express five or fewer types of transcripts, and half encode just one protein.

    “Our study indicates that the total information output of an animal transcriptome is heavily weighted by the needs of the developing nervous system,” says Ben Brown, a Berkeley Lab staff scientist in the Life Sciences Division who led the data analysis team.

    The scientists also discovered a much broader response to stress than previously recognized. Exposure to heavy metals like cadmium resulted in the activation of known stress-response pathways that prevent damage to DNA and proteins. It also revealed several new genes of completely unknown function.

    “To better understand how cells fight stress, we have to figure out what these mysterious genes do,” says Celniker.

    The research was funded by the National Human Genome Research Institute modENCODE Project.

    Other institutions involved in this research include the Sloan-Kettering Institute, Japan’s RIKEN Yokohama Institute, Cold Spring Harbor Laboratory, and Harvard Medical School.

    See the full article here.

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  • richardmitnick 5:01 pm on February 3, 2014 Permalink | Reply
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    From Berkeley Lab: “How a Shape-shifting DNA-repair Machine Fights Cancer” 


    Berkeley Lab

    February 03, 2014
    Dan Krotz 510-484-5956 dakrotz@lbl.gov

    Maybe you’ve seen the movies or played with toy Transformers, those shape-shifting machines that morph in response to whatever challenge they face. It turns out that DNA-repair machines in your cells use a similar approach to fight cancer and other diseases, according to research led by scientists from the U.S. Department of Energy’s Lawrence Berkeley National Laboratory (Berkeley Lab).

    mre
    One protein complex, two very different shapes and functions: In the top image, the scientists created an Mre11-Rad50 mutation that speeds up hydrolysis, yielding an open state that favors a high-fidelity way to repair DNA. In the bottom image, the scientists slowed down hydrolysis, resulting in a closed ATP-bound state that favors low-fidelity DNA repair. (Credit: Tainer lab)

    As reported in a pair of new studies, the scientists gained new insights into how a protein complex called Mre11-Rad50 reshapes itself to take on different DNA-repair tasks.

    Their research sheds light on how this molecular restructuring leads to different outcomes in a cell. It could also guide the development of better cancer-fighting therapies and more effective gene therapies.

    As reported in a pair of new studies, the scientists gained new insights into how a protein complex called Mre11-Rad50 reshapes itself to take on different DNA-repair tasks.

    Their research sheds light on how this molecular restructuring leads to different outcomes in a cell. It could also guide the development of better cancer-fighting therapies and more effective gene therapies.

    Mre11-Rad50’s job is the same in your cells, your pet’s cells, or any organism’s. It detects and helps fix the gravest kind of DNA breaks in which both strands of a DNA double helix are cut. The protein complex binds to the broken DNA ends, sends out a signal that stops the cell from dividing, and uses its shape-shifting ability to choose which DNA repair process is launched to fix the broken DNA. If unrepaired, double strand breaks are lethal to the cell. In addition, a repair job gone wrong can lead to the proliferation of cancer cells.

    Little is known about how the protein’s Transformer-like capabilities relate to its DNA-repair functions, however.

    To learn more, the scientists modified the protein complex in ways that were designed to affect just one of the many activities it undertakes. They then used structural biology, biochemistry, and genomic tools to study the impacts of these modifications.

    “By targeting a single activity, we can make the protein complex go down a different pathway and learn how its dynamic structure changes,” says John Tainer of Berkeley Lab’s Life Sciences Division. He conducted the research with fellow Berkeley Lab scientist Gareth Williams and scientists from several other institutions.

    Adds Williams, “In some cases, we sped up or slowed down the protein complex’s movements, and by doing so we changed its biological outcomes.”

    sybll
    Much of the research was conducted at the SIBYLS beamline at the Advanced Light Source. SIBYLS stands for Structurally Integrated Biology for Life Sciences.

    Much of the research was conducted at the Advanced Light Source (ALS), a synchrotron located at Berkeley Lab that generates intense X-rays to probe the fundamental properties of substances. They used an ALS beamline called SYBILS, which combines X-ray scattering with X-ray diffraction capabilities. It yields atomic-resolution images of the crystal structures of proteins. It can also watch the transformation of the protein as it undergoes conformational changes.

    In one study published in the journal Molecular Cell, the scientists studied Mre11 from microbial cells. They developed two molecular inhibitors that block Mre11’s ability to cut DNA, a critical initial step in the repair process.

    They tested the effect of these inhibitors in human cells. They found that Mre11 first makes a nick away from the broken DNA strand it is repairing. Mre11 then works back toward the broken end. Previously, scientists thought that Mre11 always starts at the broken DNA end. They also found that when Mre11 cuts in the middle of a DNA strand, it initiates a high-precision DNA-repair pathway called homologous recombination repair.

    In another study published in EMBO Journal, the scientists created Rad50 mutations that either promote or destabilize the shape formed when the Rad50 subunit binds with ATP, a chemical that fuels the protein complex’s movements.

    Biochemical and functional assays conducted by Tanya Paull of the University of Texas at Austin revealed how these changes affect microbial, yeast, and human Mre11-Rad50 activities. Paul Russell at the Scripps Research Institute helped the scientists learn how these Rad50 mutations affect yeast cells.

    They found that some mutations slowed down ATP hydrolysis, which is how Rad50 and other enzymes use ATP as fuel. Other mutations sped it up. Both changes affected Mre11-Rad50’s workflow, and its biological outcomes, in a big way.

    “When we slowed down hydrolysis and favored the ATP-bound state, Rad50 favored a non-homologous end joining pathway, which is a low-fidelity way to repair DNA,” says Williams. “When we sped it up, the subunit favored homologous repair, which is the high-fidelity pathway.”

    This approach, in which scientists start with a specific protein mechanism and learn how it affects the entire organism, will help researchers develop a predictive understanding of how Mre11-Rad50 works.

    “It’s a ‘bottom up’ way to study proteins such as Mre11-Rad50, and it could guide the development of better cancer therapies and other applications,” says Tainer.

    See the full article, with further material, here.

    A U.S. Department of Energy National Laboratory Operated by the University of California

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  • richardmitnick 2:58 pm on September 16, 2013 Permalink | Reply
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    From Livermore Lab: “It’s a shock: Life on Earth may have come from out of this world” 


    Lawrence Livermore National Laboratory

    09/15/2013
    Anne M Stark, LLNL, (925) 422-9799, stark8@llnl.gov

    A group of international scientists including a Lawrence Livermore National Laboratory researcher have confirmed that life really could have come from out of this world. The team shock compressed an icy mixture, similar to what is found in comets, which then created a number of amino acids – the building blocks of life. The research appears in advanced online publication Sept. 15 on the Nature Geoscience journal website.

    atoms
    Comets contain elements such as water, ammonia, methanol and carbon dioxide that could have supplied the raw materials, in which upon impact on early Earth would have yielded an abundant supply of energy to produce amino acids and jump start life.

    This is the first experimental confirmation of what LLNL scientist Nir Goldman first predicted in 2010 and again in 2013 using computer simulations performed on LLNL’s supercomputers, including Rzcereal and Aztec.

    Goldman’s initial research found that the impact of icy comets crashing into Earth billions of years ago could have produced a variety of prebiotic or life-building compounds, including amino acids. Amino acids are critical to life and serve as the building blocks of proteins. His work predicted that the simple molecules found in comets (such as water, ammonia, methanol and carbon dioxide) could have supplied the raw materials, and the impact with early Earth would have yielded an abundant supply of energy to drive this prebiotic chemistry.

    In the new work, collaborators from Imperial College in London and University of Kent conducted a series of experiments very similar to Goldman’s previous simulations in which a projectile was fired using a light gas gun into a typical cometary ice mixture. The result: Several different types of amino acids formed.

    “These results confirm our earlier predictions of impact synthesis of prebiotic material, where the impact itself can yield life-building compounds,” Goldman said. “Our work provides a realistic additional synthetic production pathway for the components of proteins in our solar system, expanding the inventory of locations where life could potentially originate.”

    See the full article here.

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  • richardmitnick 11:05 am on September 13, 2013 Permalink | Reply
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    From Berkeley Lab: “Radiotherapy in Girls and the Risk of Breast Cancer Later in Life” 


    Berkeley Lab

    September 11, 2013
    Lynn Yarris (510) 486-5375 lcyarris@lbl.gov

    Exposing young women and girls under the age of 20 to ionizing radiation can substantially raise the risk of their developing breast cancer later in life. Scientists may now know why. A collaborative study, in which Berkeley Lab researchers played a pivotal role, points to increased stem cell self-renewal and subsequent mammary stem cell enrichment as the culprits. Breasts enriched with mammary stem cells as a result of ionizing irradiation during puberty show a later-in-life propensity for developing ER negative tumors – cells that do not have the estrogen receptor. Estrogen receptors – proteins activated by the estrogen hormone – are critical to the normal development of the breast and other female sexual characteristics during puberty.

    markers
    This mammary gland agent-based model depicts the network structure at week three formed by cell agents that come together to form duct agents. In turn, duct agents organize into a network similar to the branched structure of the mammary gland. No image credit.

    “Our results are in agreement with epidemiology studies showing that radiation-induced human breast cancers are more likely to be ER negative than are spontaneous breast cancers,” says Sylvain Costes, a biophysicist with Berkeley Lab’s Life Sciences Division. “This is important because ER negative breast cancers are less differentiated, more aggressive, and often have a poor prognosis compared to the other breast cancer subtypes.”

    Costes and Jonathan Tang, also with Berkeley Lab’s Life Sciences Division, were part of a collaboration led by Mary Helen Barcellos-Hoff, formerly with Berkeley Lab and now at the New York University School of Medicine, that investigated the so-called “window of susceptibility” known to exist between radiation treatments at puberty and breast cancer risk in later adulthood. The key to their success were two mammary lineage agent-based models (ABMs) they developed in which a system is modeled as a collection of autonomous decision-making entities called agents. One ABM simulated the effects of radiation on the mammary gland during either the developmental stages or during adulthood. The other simulated the growth dynamics of human mammary epithelial cells in culture after irradiation.

    This mammary gland agent-based model depicts the network structure at week three formed by cell agents that come together to form duct agents. In turn, duct agents organize into a network similar to the branched structure of the mammary gland.

    “Our mammary gland ABM consisted of millions of agents, with each agent representing either a mammary stem cell, a progenitor cell or a differentiated cell in the breast,” says Tang. “We ran thousands of simulations on Berkeley Lab’s Lawrencium supercomputer during which each agent continually assessed its situation and made decisions on the basis of a set of rules that correspond to known or hypothesized biological properties of mammary cells. The advantage of this approach is that it allows us to view the global consequences to the system that emerge over time from our assumptions about the individual agents. To our knowledge, our mammary gland model is the first multi-scale model of the development of full glands starting from the onset of puberty all the way to adulthood.”

    Epidemiological studies have shown that girls under 20 given radiotherapy treatment for disorders such as Hodgkin’s lymphoma run about the same risk of developing breast cancer in their 40s as women who were born with a BRCA gene mutation. From their study, Costes, Tang and their collaboration partners concluded that self-renewal of stem cells was the most likely responsible mechanism.

    “Stem cell self-renewal was the only mechanism in the mammary gland model that led to predictions that were consistent with data from both our in vivo mouse work and our in vitro experiments with MCF10A, a human mammary epithelial cell line,” Tang says. “Additionally, our model predicts that this mechanism would only generate more stem cells during puberty while the gland is developing and considerable cell proliferation is taking place.”

    Costes and Tang are now looking for genetic or phenotypic biomarkers that would identify young girls who are at the greatest breast cancer risk from radiation therapy. The results of their study with Barcellos-Hoff and her research group show that the links between ionizing radiation and breast cancer extend beyond DNA damage and mutations.

    “Essentially, exposure of the breast to ionizing radiation generates an overall biochemical signal that tells the system something bad happened,” Costes says. “If exposure takes place during puberty, this signal triggers a regenerative response leading to a larger pool of stem cells, thereby increasing the chance of developing aggressive ER negative breast cancers later in life.”

    See the full article here.

    A U.S. Department of Energy National Laboratory Operated by the University of California

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  • richardmitnick 2:11 pm on August 12, 2013 Permalink | Reply
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    From Livermore Lab: "Lawrence Livermore scientists make new discoveries in the transmission of viruses between animals and humans" 


    Lawrence Livermore National Laboratory

    08/12/2013
    Kenneth K Ma

    “Outbreaks such as the severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome coronavirus (MERS) have afflicted people around the world, yet many people think these trends are on the decline. Quite the opposite is true.

    sars
    SARS coronavirus (SARS-CoV) is causative of the syndrome.

    mers
    MERS-CoV particles as seen by negative stain electron microscopy. Virions contain characteristic club-like projections emanating from the viral membrane.

    The efforts to combat this epidemic are being spearheaded by a team of Lawrence Livermore National Laboratory (LLNL) scientists. Led by Monica Borucki of LLNL’s Biosciences and Biotechnology Division, the Lab researchers have made promising new discoveries that provide insight into the emergence of inter-species transmittable viruses.

    They discovered that the genetic diversity of a viral population within a host animal could allow a virus to adapt to certain conditions, which could help it reach a human host. This discovery advances the scientific understanding of how new viruses produced from animal reservoirs can infect people. An animal reservoir is an animal species that harbors an infectious agent, which then goes on to potentially infect humans or other species. Borucki’s team is investigating viruses related to SARS and MERS, but not the actual viruses themselves.

    ‘The team’s findings are the first steps in developing methods for predicting which viral species are most likely to jump from animals to humans and potentially cause outbreaks of diseases,’ Borucki said.

    Borucki’s LLNL multidisciplinary research team includes Jonathan Allen, Tom Slezak, Clinton Torres and Adam Zemla from the Computation Directorate; Haiyin Chen from the Engineering Directorate; and Pam Hullinger, Gilda Vanier and Shalini Mabery from the Physical and Life Sciences Directorate.

    team

    Coronaviruses are one of the groups of viruses that most commonly jump to new host species as evidenced by SARS and MERS, according to Borucki. These viruses appear to have jumped from animals to humans and are capable of causing severe diseases in humans.

    ‘Our discoveries indicate that the next generation of genetic sequencing technology, combined with advance computational analysis, can be used to characterize the dynamics of certain viral populations,’ she said.”

    See the full article here.

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  • richardmitnick 9:24 pm on July 18, 2013 Permalink | Reply
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    From Berkeley Lab: “Even Bacteria Use Social Networks” 


    Berkeley Lab

    Berkeley Lab scientists image cell-to-cell connections between soil microbes

    July 18, 2013
    Dan Krotz dakrotz@lbl.gov

    “The next time your Facebook stream is filled with cat videos, think about Myxococcus xanthus. The single-cell soil bacterium also uses a social network. But forget silly distractions. M. xanthus relies on its connections to avoid getting eaten and to score its next meal.

    mx
    An extensive network of cell-to-cell connections (shown in red) is seen in this 3-D rendering of M. xanthus which is imaged by focused ion beam scanning electron microscopy. (Credit: Auer lab)

    That’s the latest insight from a team of Berkeley Lab scientists. Using several imaging techniques, they saw for the first time that M. xanthus cells are connected by a network of chain-like membranes.

    The scientists believe M. xanthus uses its network to quietly transfer proteins and other molecules from one to another. This could enable the bacteria to coordinate social activities—such as evading bacterial enemies and snaring prey—without revealing its location.

    ‘The network could be a mode of stealth communication,’ says Manfred Auer of Berkeley Lab’s Life Sciences Division. ‘M. xanthus faces stiff competition and has a lot of enemies, so it pays to keep a low profile.’

    Although the research focused on M. xanthus, it could shed light on how other bacteria work together to pull off important processes, such as breaking down plant material for biofuel production or cleaning up underground toxins. It could also lead to new antibiotics that stop harmful bacteria by knocking out their communication systems.

    The work is published online in the journal Environmental Microbiology.”

    See the full article here.

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  • richardmitnick 2:54 pm on March 22, 2013 Permalink | Reply
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    From Berkeley Lab: “Computer Simulations Yield Clues to How Cells Interact With Surroundings” 


    Berkeley Lab

    Berkeley Lab research has implications for cancer, atherosclerosis research

    March 21, 2013
    Dan Krotz

    Your cells are social butterflies. They constantly interact with their surroundings, taking in cues on when to divide and where to anchor themselves, among other critical tasks.

    This networking is driven in part by proteins called integrin, which reside in a cell’s outer plasma membrane. Their job is to convert mechanical forces from outside the cell into internal chemical signals that tell the cell what to do. That is, when they work properly. When they misfire, integrins can cause diseases such as atherosclerosis and several types of cancer.

    integrin
    Computer models offer a new look at the molecular machinery that enables cells to interact with their environment. This schematic shows two integrin components (red and blue) protruding from a cell membrane. (Credit: Mofrad lab)

    Despite their importance—good and bad—scientists don’t exactly know how integrins work. That’s because it’s very difficult to experimentally observe the protein’s molecular machinery in action. Scientists have yet to obtain the entire crystal structure of integrin within the plasma membrane, which is a go-to way to study a protein’s function. Roadblocks like this have ensured that integrins remain a puzzle despite years of research.

    But what if there was another way to study integrin? One that doesn’t rely on experimental methods? Now there is, thanks to a computer model of integrin developed by Berkeley Lab researchers. Like its biological counterpart, the virtual integrin snippet is about twenty nanometers long. It also responds to changes in energy and other stimuli just as integrins do in real life. The result is a new way to explore how the protein connects a cell’s inner and outer environments.

    ‘We can now run computer simulations that reveal how integrins in the plasma membrane translate external mechanical cues to chemical signals within the cell,’ says Mohammad Mofrad, a faculty scientist in Berkeley Lab’s Physical Biosciences Division and associate professor of Bioengineering and Mechanical Engineering at UC Berkeley. He conducted the research with his graduate student Mehrdad Mehrbod.

    They report their research in a recent issue of PLoS Computational Biology.

    Their ‘molecular dynamics’ model is the latest example of computational biology, in which scientists use computers to analyze biological phenomena for insights that may not be available via experiment. As you’d expect from a model that accounts for the activities of half a million atoms at once, the integrin model takes a lot of computing horsepower to pull off. Some of its simulations require 48 hours of run time on 600 parallel processors at the U.S. Department of Energy’s (DOE) National Energy Research Scientific Computing Center (NERSC), which is located at Berkeley Lab.

    The model is already shedding light on what makes integrin tick, such as how they know’ to respond to more force with greater numbers. When activated by an external force, integrins cluster together on a cell’s surface and join other proteins to form structures called focal adhesions. These adhesions recruit more integrins when they’re subjected to higher forces. As the model indicates, this ability to pull in more integrins on demand may be due to the fact that a subunit of integrin is connected to actin filaments, which form a cell’s skeleton.

    ‘We found that if actin filaments sustain more forces, they automatically bring more integrins together, forming a larger cluster,’ says Mehrbod.

    The model may also help answer a longstanding question: Do integrins interact with each other immediately after they’re activated? Or do they not interact with each other at all, even as they cluster together?

    ‘Our research sets up an avenue for future studies by offering a hypothesis that relates integrin activation and clustering,’ says Mofrad.”

    See the full article here.

    A U.S. Department of Energy National Laboratory Operated by the University of California

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  • richardmitnick 10:42 am on October 16, 2012 Permalink | Reply
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    From Berkeley Lab: “New Insights Into How Genetic Differences Among Individuals Influence Breast Cancer Risk from Low-Dose Radiation” 


    Berkeley Lab

    Berkeley Lab research could lead to new ways to ID women who have higher risk of breast cancer from low-dose radiation

    October 15, 2012
    Dan Krotz

    Scientists from the U.S. Department of Energy’s Lawrence Berkeley National Laboratory (Berkeley Lab) have identified tissue mechanisms that may influence a woman’s susceptibility or resistance to breast cancer after exposure to low-dose ionizing radiation, such as the levels used in full-body CT scans and radiotherapy.

    two men
    Andy Wyrobek (left) and Antoine Snijders [of Berkeley Lab’s Life Sciences Division are among a team of Berkeley Lab scientists that is exploring the connection between genetic differences, tissue mechanisms, and women’s susceptibility to breast cancer after exposure to low-dose radiation.

    The findings also support the idea that a person’s genes play a big role in determining her risk of breast cancer from low-dose radiation. The current model for predicting cancer risk from ionizing radiation holds that risk is directly proportional to dose. But there’s a growing understanding that this linear relationship doesn’t apply at lower doses. Instead, the health effects of low-dose radiation may vary substantially among people depending on their genetic makeup.”

    Breast Cancer awareness and research have both increased exponentially in recent years. See the full very important article here. This is an area of research wherein even small steps can be very significant.

    A U.S. Department of Energy National Laboratory Operated by the University of California

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  • richardmitnick 1:56 pm on September 17, 2012 Permalink | Reply
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    From Berkeley Lab: “First 3-D Model of a Protein Critical to Embryo Development” 


    Berkeley Lab

    THIS IS A REALLY BIG DEAL

    September 14, 2012
    Lynn Yarris

    The first detailed and complete picture of a protein complex that is tied to human birth defects as well as the progression of many forms of cancer has been obtained by an international team of researchers led by scientists with the U.S. Department of Energy (DOE)’s Lawrence Berkeley National Laboratory (Berkeley Lab). Knowing the architecture of this protein, PRC2, for Polycomb Repressive Complex 2, should be a boon to its future use in the development of new and improved therapeutic drugs.

    image
    The PRC2-AEBP2 complex consists of four different lobes (A, B, C, D) interconnected by two narrow arms (Arm1, Arm2). Two activity-controlling elements of PRC2 are shown in blue and located at opposite ends. No image credit.

    ‘We present a complete molecular organization of human PRC2 that offers an invaluable structural context for understanding all of the previous biochemical and functional data that has been collected on this complex,’ says Berkeley Lab biophysicist Eva Nogales, an electron microscopy expert who led this research. ‘Our model should also be an invaluable tool for the design of new experiments aimed at asking detailed questions about the mechanisms that enable PRC2 to function and how those mechanisms might be exploited.’ “

    A U.S. Department of Energy National Laboratory Operated by the University of California

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  • richardmitnick 10:50 am on August 28, 2012 Permalink | Reply
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    From Berkeley Lab: “Nutrition Tied to Improved Sperm DNA Quality in Older Men” 


    Berkeley Lab

    August 27, 2012
    Dan Krotz

    A new study led by scientists from the U.S. Department of Energy’s Lawrence Berkeley National Laboratory (Berkeley Lab) found that a healthy intake of micronutrients is strongly associated with improved sperm DNA quality in older men. In younger men, however, a higher intake of micronutrients didn’t improve their sperm DNA.

    image
    Berkeley Lab’s Andy Wyrobek led a research team that linked nutrition to improved sperm DNA quality in older men.

    In an analysis of 80 healthy male volunteers between 22 and 80 years of age, the scientists found that men older than 44 who consumed the most vitamin C had 20 percent less sperm DNA damage compared to men older than 44 who consumed the least vitamin C. The same was true for vitamin E, zinc, and folate.

    [This] research comes as more men over 35 have children, which raises public health concerns. Previous research conducted in Wyrobek’s lab found that the older a man is, the more he’s likely to have increased sperm DNA fragmentation, chromosomal rearrangements, and DNA strand damage. Older men are also more likely to have increased frequencies of sperm carrying certain gene mutations, such as those leading to dwarfism. These findings help explain why aging men are less fertile and are predicted to have more chromosomally defective pregnancies and a higher proportion of offspring with genetic defects.”

    See the full article here.

    A U.S. Department of Energy National Laboratory Operated by the University of California

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