Water, Water, Everywhere... But Is It Safe To Drink?

"Over the last couple of generations, there has been a huge amount of groundwater pollution worldwide, and this has had a negative impact on our drinking water supply," says Barbara Sherwood Lollar, Canada Research Chair in Isotope Geochemistry of the Earth and the Environment at the University of Toronto.



Sherwood Lollar took part in the THINK CANADA Press Breakfast at AAAS. Her research examines society's efforts to reverse and stop groundwater pollution, and the effectiveness of bioremediation technologies - using microbes to clean up organic contaminants such as petroleum hydrocarbons (oil, gasoline or diesel) or chemicals used in the electronics or transportation industries.



While the disposal of these organic contaminants tends to be well regulated today, this has not always been the case. Lax regulations and enforcement during the period immediately after the Second World War has left Europe and North America with a legacy of past contamination.



"This contamination has had a pervasive impact on the environment," says Sherwood Lollar. "It is still out there, and it needs to be dealt with."



Over the past decade, many techniques used to clean up groundwater contamination have harnessed the power of microbiology and the work of geochemists like Sherwood Lollar. "We are not genetically engineering microbes," she explains. "In many settings, naturally occurring microbes feed off the organic contaminants and, in the process, convert them to non-toxic end products."



Until now, the real difficulty has been in proving that the process exists and that the microbes are actually cleaning up the contaminants. Sherwood Lollar has developed techniques that show where the clean-up is happening and, just as importantly, where it is not.



"Elements like carbon have different stable isotopes: Carbon-12 and Carbon-13. One is slightly heavier than the other, and the microbes tend to feed mostly on the lighter one. When the microbes have been working for some time, the ratio of heavy-to-light carbon will change. It is this change - referred to as an isotopic signature - that lets us know the water is being cleaned up," says Sherwood Lollar.



By cleaning up contaminated groundwater, it is possible to recuperate what would otherwise be a lost resource. The technique is starting to be used by regulators, and Sherwood Lollar is working with an international group of scientists to put together a guidance document for the United States Environmental Protection Agency (EPA).



This will provide a set of recommendations about use in the field for practitioners, which will be a first step towards mainstreaming the technique.



"It's a common misconception that water - and especially our supply of groundwater - is a renewable resource," says Sherwood Lollar. "But it isn't. So, it is particularly important that we manage it well and that we do whatever we can to conserve, protect and remediate what we have."



Source:

Michael Adams

Natural Sciences and Engineering Research Council

Regenerative Activity In The Peripheral Nervous System Could Mean Regeneration For The Central Nervous System

Researchers at the Peninsula Medical School in the South West of England, University College London, the San Raffaele Scientific Institute in Milan and Cancer Research UK, have for the first time identified a protein that is key to the regeneration of damage in the peripheral nervous system and which could with further research lead to understanding diseases of our peripheral nervous systems and provide clues to methods of repairing damage in the central nervous system, according to a paper published this week in the Journal of Cell Biology.



The team looked at a protein called c-Jun, a transcription factor that regulates the expression of other genes. They found that the c-Jun protein plays a vital role in the regulating the plasticity of Schwann cells which is vital for the way in which the peripheral nervous system regenerates and repairs itself after injury.



Schwann cells produce the sheaths that surround and insulate neurons. When there is damage to the peripheral nervous system Schwann cells unwrap themselves from the degenerating axon. During this process of repair, Schwann cells then provide the correct environment for the neurons to re-grow and complete the process of repair.



By identifying this transcription factor, the research team believes that there is scope to produce eventual cures for damage and diseases of the peripheral nervous system, such as the inherited condition Charcot-Marie-Tooth disease and the autoimmune disorder Guillain-Barre disease.



Unlike the peripheral nervous system, the central nervous system does not regenerate when damaged. With further research, the team hopes to work towards identifying ways in which Schwann cells and c-Jun could be used to repair the spinal cord, leading to possible cures and relief for millions of people around the world suffering from damage of the central nervous system.



Further research could also identify whether abnormal activation of the c-Jun protein may be involved in causing Schwann cell tumours, for instance in the condition of neurofibromatosis type 2, leading to a better understanding of this condition and the development of therapies for this condition.



Dr. David Parkinson from the Peninsula Medical School, who was lead researcher on the paper, commented: "This is a very exciting first step towards understanding how the peripheral nervous system repairs itself, how that process could be used to produce cures for diseases of and damage to the peripheral nervous system, and how it could ultimately encourage the central nervous system to behave like the peripheral nervous system and repair itself."



He added: "We knew that Schwann cells, unlike other cells in the body, are constantly able to rejuvenate themselves. We now have a better understanding of how this happens, and that understanding could be used to create treatments and therapies for a wide range of degenerative diseases."







The Peninsula Medical School is a joint entity of the University of Exeter, the University of Plymouth and the NHS in the South West of England, and a partner of the Combined Universities in Cornwall. The Peninsula Medical School has created for itself an excellent national and international reputation for groundbreaking research in the areas of diabetes and obesity, neurological disease, child development and ageing, clinical education and health technology assessment.



Source: Andrew Gould


The Peninsula College of Medicine and Dentistry

$3M From NIDA To Support Effective Prevention, Treatment And Service Strategies For Drug Abusing Youth And Adults

The Center for Proteomics and Bioinformatics and the Case Center for AIDS Research at Case Western Reserve University School of Medicine have a received a $989,108 grant from the National Institute of Drug Abuse (NIDA) at the National Institute of Health (NIH), with the ability to receive a total of $3,007,946 by 2011. The grant will allow the Center for Proteomics and Bioinformatics to expand its activities in the HIV/AIDS area, which already represents approximately 30 percent of its projects, while providing the Center for AIDS Research an opportunity to introduce advanced proteomic technology into its research portfolio. Together, the centers will study the effects of drug use on the biology of HIV/AIDS.



The new grant, over three years of funding (2009: $989,108; 2010: $1,004,415; 2011: $1,014,423), will allow the development of reliable proteomic and epigenetic biomarkers (certain proteins that can be measured as an indicator of or to better understand the progression of a disease) for chronic immune activation during HIV disease and it will help the Centers better understand the effects of current or prior drug use and Hepatitis C-co infection (HCV) on disease progression and therapy. The grant also will provide funding for technology development in proteomics and systems biology research tools, further cementing existing collaborative relationships between CFAR investigators at the School of Medicine, the Dental school, the Louis Stokes VA hospital and investigators at the Center for Proteomics and Bioinformatics.



"There is a pressing need to obtain objective measurements of how HIV disease progresses and to investigate whether drug abuse alters the course of HIV disease," said Jonathan Karn, chair of the Department of Molecular Biology & Microbiology, director of the Case Center for AIDS Research (CFAR), and co-PI on the study. "Currently patients under HAART (anti-viral) therapy show a wide range of clinical outcomes, but physicians lack reliable indicators of how HIV disease progresses."



The AIDS Clinical Trials Unit, through the School of Medicine and University, provides both centers ample access to specimens needed to conduct this study.



"We will develop several pilot projects in collaboration with the CFAR investigator team to explore the proteomes of patients who have HIV or HCV, who may be on anti-retroviral therapy, and who may be drug users or in drug treatment programs," said Mark Chance, director, Center for Proteomics and Bioinformatics and lead PI of the study. "At the same time, specific changes in genes or epigenetic changes will also be explored. A Proteomics and Bioinformatics core will support these pilot projects with study design and biostatistical expertise, proteomics services, and systems biology data analysis."
















During the pilot phase, the Center will fund and coordinate a set of inter-related projects designed to provide a better understanding of the impact on immune function and activity in HIV-infected individuals who are also exposed to addictive drugs, and the importance of viral HCV. In each of these projects there will be a direct examination of the proteomic responses in either cells lining the digestive tract or immune cells and parallel examination of plasma readouts from affected patients.



The data will be rationalized using techniques to identify specific inflammatory pathways that are activated. Technologies for analyzing epigenetic changes in the immune system will be developed, with a goal of being able to correlate changes in the genome with those in the proteome. The ultimate goal of these projects will be the development of informative biomarkers and methods that can be used in large-scale population studies to further evaluate the impact of drug use on HIV disease.



"We are delighted to be able to initiate new research in this area and welcome the innovative leadership that NIDA is providing to study of the molecular basis of the interactions between drug use and HIV disease," said Chance. "This grant is important from an institutional perspective as well because it will introduce Case's advanced proteomics and systems biology capacities to NIDA, and provide investigators who are currently studying HIV/AIDS with an excellent opportunity to identify and study their drug abuse cohorts."



Needle sharing and/or impaired decision-making resulting from intoxication that can lead to risky sexual behaviors, often lead drug users to contract HIV/AIDS; the number of HIV patients who use or have used drugs is 10-30 percent. Better approaches to understanding their HIV/AIDS progression and developing treatments specific to their conditions is a specific goal of the research.



Source:
Christina DeAngelis


Case Western Reserve University

Biophysical Society Selects 2009 Distinguished Service, Emily M. Gray And Society Fellow Recipients

The Biophysical Society is pleased to announce the recipients of its 2009 Distinguished Service Award and the Emily M. Gray Award, as well as the Society's 2009 Fellows. All of the award winners and Fellows will be recognized at the Awards Ceremony during the Biophysical Society's 53rd Annual Meeting on Monday March 2, 2009 at the Boston Convention and Exhibition Center in Boston, Massachusetts.



Jeremy M. Berg of the National Institute of General Medical Sciences, NIH, will receive the Distinguished Service Award for his active and continuous support for biomedical research in general, and biophysics in particular, and the successful and creative leadership he has demonstrated in these activities. His longstanding support stems from his deep knowledge in the sciences basic to medicine and health, anchored in his own research career and the important contributions he has made to understanding the structural and functional roles of proteins in key physiological functions. The Distinguished Service Award, established by the Biophysical Society, honors service in the field of biophysics and for contributions beyond achievements in research.



Philip C. Nelson, University of Pennsylvania, will receive the Emily M. Gray Award for his far reaching and significant contributions to the teaching of biophysics, developing innovative educational materials, and fostering an environment exceptionally conducive to education in Biological Physics. The Award is given for significant contributions to education in biophysics whether by teaching, developing novel educational methods or materials, promoting scientific outreach efforts to the public or to youth, generating a track record of attracting new students to the field of biophysics, or by otherwise fostering an environment exceptionally conducive to education in biophysics.



Five Biophysical Society members have been named to the 2009 class of Society Fellows. This award is designed to honor the Society's distinguished members who have demonstrated excellence in science and to the expansion of the field of biophysics. The Fellows are:

Donald M. Bers, University of California, Davis, for his contributions to the field of cellular and molecular biology of excitation contraction and coupling in the heart;



Betty Gaffney, Florida State University, for being in the investigative forefront of spin labeling technology and electron paramagnetic resonance, the structure and dynamics of biological membranes, and the mechanisms of lipoxygenase function;



Robert Jernigan, Baker Center for Bioinformatics & Computational Biology Plant Sciences Institute, Iowa State University, for his distinguished research and leadership in coarse-grained studies of proteins and their interactions;



Mark T. Nelson, University of Vermont, for his important contributions to explaining complex physiological processes in smooth muscle function; and



Diane Papazian, David Geffen School of Medicine, UCLA, for her contributions to the physiology and biophysics of ion channels and how mutation in such channels are linked to diseases.





The Biophysical Society, founded in 1956, is a professional, scientific society established to encourage development and dissemination of knowledge in biophysics. The Society promotes growth in this expanding field through its annual meeting, monthly journal, and committee and outreach activities. Its 8200 members are located throughout the U.S. and the world, where they teach and conduct research in colleges, universities, laboratories, government agencies, and industry. For more information on the society or the 2009 annual meeting, visit biophysics/.



Source: Ellen R. Weiss


Biophysical Society

Space Versus Phylogeny: Disentangling Phylogenetic And Spatial Signals In Comparative Data

Variation in traits across species or populations is the outcome of both environmental and historical factors.


Trait variation is therefore a function of both the phylogenetic and spatial context of species. Here we introduce a method that within a single framework estimates the relative roles of spatial and phylogenetic variation in comparative data.


The approach requires traits measured across phylogenetic units, e.g. species, the spatial occurrences of those units and a phylogeny connecting them.


Proceedings of the Royal Society B: Biological Sciences


Proceedings B is the Royal Society's flagship biological research journal, dedicated to the rapid publication and broad dissemination of high-quality research papers, reviews and comment and reply papers. The scope of journal is diverse and is especially strong in organismal biology.


Proceedings of the Royal Society B: Biological Sciences

New Way To Assemble Artificial Tissues Created By Tissue Engineers

Tissue engineering has long held promise for building new organs to replace damaged livers, blood vessels and other body parts. However, one major obstacle is getting cells grown in a lab dish to form 3-D shapes instead of flat layers.



Researchers at the MIT-Harvard Division of Health Sciences and Technology (HST) have come up with a new way to overcome that challenge, by encapsulating living cells in cubes and arranging them into 3-D structures, just as a child would construct buildings out of blocks.



The new technique, dubbed "micromasonry," employs a gel-like material that acts like concrete, binding the cell "bricks" together as it hardens. Ali Khademhosseini, assistant professor of HST, and former HST postdoctoral associate Javier Gomez Fernandez describe the work in a paper published online in the journal Advanced Materials.



The tiny cell bricks hold potential for building artificial tissue or other types of medical devices, says Jennifer Elisseeff, associate professor of biomedical engineering at Johns Hopkins University, who was not involved in the research. "They're very elegant and have a lot of flexibility in how you grow them," she says. "It's very creative."



To obtain single cells for tissue engineering, researchers have to first break tissue apart, using enzymes that digest the extracellular material that normally holds cells together. However, once the cells are free, it's difficult to assemble them into structures that mimic natural tissue microarchitecture.



Some scientists have successfully built simple tissues such as skin, cartilage or bladder on biodegradable foam scaffolds. "That works, but it often lacks a controlled microarchitecture," says Khademhosseini, who is also an assistant professor at Brigham and Women's Hospital. "You don't get tissues with the same complexity as normal tissues."



The HST researchers built their "biological Legos" by encapsulating cells within a polymer called polyethylene glycol (PEG), which has many medical uses. Their version of the polymer is a liquid that becomes a gel when illuminated, so when the PEG-coated cells are exposed to light, the polymer hardens and encases the cells in cubes with side lengths ranging from 100 to 500 millionths of a meter.



Once the cells are in cube form, they can be arranged in specific shapes using templates made of PDMS, a silicon-based polymer used in many medical devices. Both template and cell cubes are coated again with the PEG polymer, which acts as a glue that holds the cubes together as they pack themselves tightly onto the scaffold surface.



After the cubes are arranged properly, they are illuminated again, and the liquid holding the cubes together solidifies. When the template is removed, the cubes hold their new structure.



Gomez Fernandez and Khademhosseini used this method to build tubes that could function as capillaries, potentially helping to overcome one of the most persistent problems with engineered organs - lack of an immediate blood supply. "If you build an organ, but you can't provide nutrients, it is going to die," says Gomez Fernandez, now a postdoctoral fellow at Harvard. They hope their work could also lead to a new way to make artificial liver or cardiac tissue.



Other researchers have developed a technique called organ printing to create complex 3-D tissues, but that process requires a robotic machine that is not in widespread use. The new technique does not require any special equipment. "You can reproduce this in any lab," says Gomez Fernandez. "It's very simple."



To get to the point where these engineered tissues could become clinically useful, "the short-term next step is really looking at different cell types and the viability of tissue growth," says Elisseeff. The researchers are now doing that, and they are also exploring the use of different polymers that could replace PEG and offer more control over cell placement.



Source:

Jennifer Hirsch

Massachusetts Institute of Technology

Protein's Role In Cancer Spread Pinpointed By Study

Edinburgh scientists have identified the way a specific cell protein can trigger the spread of cancer. The study by researchers in the Cell Signalling Unit, University of Edinburgh Cancer Research Centre could pave the way for new drugs which limit the protein's ability to turn a normal cell cancerous.



The protein, MDM2, normally functions to control the activity of a key cancer preventing protein called p53. In some of the body's cells, the biochemical ratio between MDM2 and p53 can become unbalanced causing MDM2 to act as a cancer-promoting agent.



The project's lead investigator, Dr Kathryn Ball, a researcher at the University, explains: "One way in which MDM2 controls the p53 protein is by activating its destruction and we are interested in understanding how this happens at a biochemical level.



"In the current study, funded by Cancer Research UK, we have identified protein fragments which can bind to MDM2, inhibiting its activity. These fragments could be a good template for drugs designed to hinder the role of MDM2 in the p53 destruction pathway. We hope our findings may lead to improved treatments for a broad range of cancer types."



Welcoming the findings, Professor John Toy, medical director at Cancer Research UK, said: "p53 is a crucial protein that acts as a guardian of the normal cell. Its failure to do its job properly is associated with many types of cancer. If p53 is being destroyed by another protein in a cancer cell, then it offers an excellent target when designing new anti-cancer drugs. This research suggests MDM2 is just such a target."







The study is published in the current edition of Molecular Cell.



Contact: Linda Menzies


University of Edinburgh