Emily McFadden, a Westhampton College junior and biochemistry major, recently received the national Beckman Scholarship for outstanding undergraduate research in the chemistry and biological sciences.

The Beckman Scholars Program , established in 1997, was designed to provide scholarships that contribute significantly in advancing the education, research training and personal development of select students in biochemistry and its relative fields, according to the programs website. The nationwide scholarship is awarded to six undergraduate students each year.

McFadden, one of the six students selected to receive the scholarship in 2012 , said the $19,200 grant would cover her research costs for the next two summers and her senior year.

The grant funds travel to symposiums and conferences across the country where I can present my research, McFadden said. It also plays for supplies in my lab.

McFaddens research, which she has been conducting for the past year and a half, takes place in a Gottwald biochemistry lab with the help of a faculty mentor.

Ive been researching a specific enzyme involved in DNA repair, McFadden said. My upcoming project is looking at an alternative enzyme, and comparing the two to see how their efficiency in DNA repair is different.

McFadden said the final culmination of her research would take place next summer, when she would present her project results at the Beckman Scholars Conference in California.

Ill have the opportunity to show my work to the members of the Beckman Foundation, as well as any other scientists who may be interested in my findings, McFadden said.

Michelle Hamm , associate professor of chemistry at the University of Richmond , serves as McFaddens mentor and nominated McFadden to receive the scholarship.

Emily is a bright and talented student with a passion for science, Hamm said. The Beckman award is for future scientific leaders, and I thought that description fit Emily well.

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Westhampton junior receives national research scholarship

Public release date: 27-Mar-2012 [ | E-mail | Share ]

Contact: Jan Zverina jzverina@sdsc.edu 858-534-5111 University of California - San Diego

A graduate student working in the Walker Molecular Dynamics laboratory at the San Diego Supercomputer Center (SDSC) at the University of California, San Diego is a recipient of the 2012-2013 NVIDIA Graduate Fellowship Program award for his innovative molecular dynamics research using GPU (graphics processing unit) computing.

Benjamin Madej, a chemistry and biochemistry Ph.D. student at UC San Diego, will receive a $25,000 scholarship to further his research. Madej received his Bachelor of Science in biomedical engineering from Washington University in St. Louis, Missouri, and is currently working on new methods for developing force fields used in molecular dynamics software, specifically the AMBER MD package.

Madej's research proposal focused on not only improving the AMBER Molecular Dynamics GPU engine, but extending the use of GPUs to multiple facets of molecular dynamics development and workflow for new drug discovery.

"We are proud of Ben's achievement in being awarded this prestigious scholarship and recognition," said SDSC Director Michael Norman. "It is very gratifying to see such a high level of accomplishment in computational science as Ben pursues his doctorate here at UC San Diego."

"This fellowship is a testimony to Ben's past work, the importance of GPUs at the frontiers of molecular dynamics and drug discovery, and recognition of the future potential of his contributions to science. The GPU revolution is transforming the field and this fellowship provides vital support for us to continue this cutting-edge research," said Ross C. Walker, an assistant research professor with SDSC and head of the Walker Molecular Dynamics laboratory. Walker also is an adjunct assistant professor in UC San Diego's Department of Chemistry and Biochemistry, as well as an NVIDIA CUDA Fellow.

The NVIDIA Graduate Fellowship Program provides funding to Ph.D. students who are researching topics that will lead to major advances in the graphics and high-performance computing industries, and are investigating innovative ways of leveraging the power of GPUs. Recipients not only receive crucial funding for their research, but are provided access to NVIDIA products, technology, and expertise.

"This year the NVIDIA Foundation joined in our search for top Ph.D. students who are investigating innovative ways to leverage the power of the GPU, especially those that will ultimately benefit humanity," said Chandra Cheij, NVIDIA's research program manager. "Congratulations to Ben and SDSC for this significant achievement."

SDSC's Walker Molecular Dynamics lab is focused on computational chemistry, molecular biology, and high-performance computing. The lab is particularly interested in the development of efficient algorithms for parallel computation of Quantum Mechanical and hybrid Quantum/Molecular Mechanical (QM/MM) techniques, as well as improvements in the computational efficiency and accuracy of classical MM dynamics simulations.

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SDSC graduate student awarded NVIDIA Graduate Fellowship

Newswise Cigarette smoke cannot only cause cancer, but it's also responsible for the spread of it, according to research by UC Merced biochemistry Professor Henry Jay Forman.

Forman discovered tobacco smoke activates an enzyme called Src that causes cancer cells to spread to other parts of the body. The study will appear in the April 15 edition of Free Radical Biology and Medicine.

Cigarette smoke is the major cause of lung cancer, Forman said, but nearly half of lung cancer patients remain active smokers. Nonetheless, researchers haven't understood how cigarette smoke causes cancer to metastasize.

The lab was also able to prevent cigarette smoke from activating the enzyme by introducing an antioxidant. Forman's discovery could prove useful in the fight against cancer, as it creates more understanding on how it spreads and how antioxidants can help combat this.

Forman will present his findings on April 21 at the Experimental Biology 2012 conference in San Diego.

Forman coauthored the paper with a professor from the University of Padova in Italy. Forman served as a visiting professor during the summer while also conducting research.

In another paper, recently published in the Journal of Biological Chemistry, Forman collaborated with investigators at USC who are experts in looking at how cells maintain themselves using proteasome, which degrades old and damaged proteins. When cells are under oxidative stress, the proteasomes work faster to remove damaged proteins.

However, the lab discovered the signal used to increase a cell's defenses doesn't happen in old age, causing cells to die and turn malignant. The findings offer more insight into age-related problems, such as Alzheimer's disease. Both studies were supported by the National Institutes of Health.

Forman will continue his research this summer, focusing on three projects: understanding how differences in the expression of a particular enzyme increases human susceptibility to air pollution; studying how people with sickle cell trait may have a sickle cell crisis when doing severe exercise; and studying how cigarette smoke activates an enzyme that regulates changes in lung cancer cells that promote metastasis. The three projects are also funded by the National Institutes of Health.

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Continued Smoking Can Spread Cancer

Senior Naomi Lopez, 18, is one of Sterling High Schools January Students of the Month. Her mother is Veronica Jaramillo, 38, and her brother is Elias Moreno, 9; they live in Sterling.

Favorite class: AP U.S. history. Its rigorous, and theres always something to read.

Top teacher: Susan Lawson, AP literature. Shes relatable, and she really cares about teaching us to become better readers and writers.

Extracurriculars: Tennis, I used to cheerlead. I played soccer freshman year.

After graduation: I want to major in biochemistry or molecular biology. I want to be a cosmetic dermatologist, a facial plastic surgeon or a pathologist.

Paycheck: I work off and on at Karlins Hallmark in Sterling. I was seasonal this year. I like it. Its really festive in there.

Best friend: Dahley Vinson. Shes funny, witty. She knows how to listen.

Favorite musical group: Empire of the Sun.

Favorite actor: Vincent Cassel.

Favorite movies: Black Swan and When Harry Met Sally.

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Sterling Student of the Month

Submitted March 26, 2012 4:02PM

NIU Professor Tao Xu, who has developed a promising nanoscience research program in solar energy conversion, is getting a grant from the National Science Foundation. NSF has awarded the chemistry and biochemistry professor, who lives in west suburban Lisle, with a prestigious Faculty Early Career Development grant of $400,000 over the next five years in support of his research and teaching efforts. | Submitted by NIU

storyidforme: 27984965 tmspicid: 10105310 fileheaderid: 4658715

Updated: March 26, 2012 4:02PM

NIU Professor Tao Xu, who has developed a promising nanoscience research program in solar energy conversion, is getting a big boost from the National Science Foundation.

NSF has awarded the chemistry and biochemistry professor with a prestigious Faculty Early Career Development (CAREER) grant of $400,000 over the next five years in support of his research and teaching efforts.

CAREER awards support junior faculty who exemplify the role of teacher-scholars through outstanding research, excellent education and the integration of education and research.

This award is a tribute to the quality and productivity of Dr. Xu and his research group, said Jon Carnahan, chair of the department of chemistry and biochemistry. Were very proud of Taos accomplishment.

Xu, of Lisle, also is affiliated with NIUs Institute for Nano Science, Engineering, and Technology. His research group is working to develop potential solar cells of the future.

Because of environmental concerns related to nuclear and fossil-fuel-based energy, people are demanding clean alternative energies that can help build up our power grids, Xu said. Solar cells are quite safe, but we need to enhance their overall efficiency and affordability. To accomplish this, our group is trying to gain a better understanding of the fundamental processes at work in solar cells.

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NIU chemistry professor receives grant from National Science Foundation

Many University students will travel abroad this summer, but only two funded by the Honors International Scholars Program will travel toChinato study medicine.

JuniorMuhan Huand sophomoreMatthew Hess,biochemistry majors from Augusta, will leave for Beijing in June. From there they will travel toKaifeng,China,where they will shadow doctors in the city hospital. The couple will also visit a small village outside of the city to experience the differences between a big city hospital and a small town clinic.

Muhan Hu and her boyfriend Matt are going on a trip to China funded by the Honors program to learn about medicine in Asia. KATHRYN INGALL/Staff

TheHonors International Scholars Programis an award program granted to second and third year honors students through competitive application to support them so they may travel abroad.

We dont want lack of money to prevent students from studying abroad, saidMaria de Rocher, coordinator of honors programming. We select students depending on the money we have available, usually around 35 to 45 students. This year we were able to award scholarships to 50, so thats a great number we have been able to award.

De Rocher said the scholarship gets funding from individual donations, and applications are due in early November for travel the following year.

Students who apply can choose an already existing program or can make their own program. During the application process, students write a proposal of what they will do and from that they are judged on whether the idea is worth funding.

Hu and Hess chose to make their own program studying different types of medicine inChina, because Hu was able to connect with people there who could help her reach this goal.

The big challenge was actually getting in touch with someone inChinawho would sponsor us while we were there, Hu said. I do not foresee any huge problems once we get there. I am fluent in Chinese, but I think Matt might have a harder time since he doesnt speak the language.

Hu, who is originally fromChina, said she is enthusiastic about going back to be able to tour the country and see the sites with Hess while studying medicine there.

Continued here:
Students create their own study abroad program to China

By Stephen Brooks | Originally Published: 1 hour ago |Modified: 1 hour ago |

Biochemistry professor Rawle Hollingsworth in his lab on Wednesday March 9, 2005.

During biochemistry professor Rawle Hollingsworths nearly 30 years at MSU, Tom Sharkey, chair of the biochemistry and molecular biology department, remembers having many conversations with him during casual run-ins outside the office.

One encounter sticks out in Sharkeys mind, who said he has a strong memory of listening to Hollingsworth explain carbohydrate involvement in blood types one day in the parking lot.

I was just fascinated to learn the things he was explaining, Sharkey said. Its just one of those moments in time that get frozen for reasons that you dont really know why.

Hollingsworth, a 55-year-old Haslett, Mich. resident, died from a pulmonary embolism on Feb. 29.

After completing his doctorate at the University of the West Indies in the Caribbean, Hollingsworth started as an assistant professor at MSU in 1983 and climbed the ranks to become a full professor.

I would say his enthusiasm really was the thing I continually think about when I think of him, Sharkey said.

Rawle Hollingsworth met his wife, Saleela Hollingsworth, at the University of the West Indies. The two were married for 26 years and had two children, Misha, 20, and Akhil, 15.

Saleela Hollingsworth said her husband loved traveling, reading and music and always put the childrens interests first.

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Professor leaves positive legacy

Mark Merchant, biochemistry professor at McNeese State University, spoke with Leesville High School students Tuesday to discuss his ongoing research project investigating naturally occurring antibacterial peptides in alligators to uncover a new class of antibiotics. Merchant said he was first interested in this research when he noticed alligators who sustained serious injuries, such as a missing limb or tail, would not only heal rapidly, but also without any infections. So he set out to investigate in marshes to collect blood samples from crocodilians, which includes all alligator, crocodile and caiman species, to study their tissue and immune systems. After extracting the white blood cells, Merchant infused them with bacteria and discovered holes where it did not grow, proving there is something inside their white blood cells that kill bacteria. Merchant derived the term Zone of Inhibition to explain the area where bacteria cannot grow as well as measure the zone towards a variety of bacteria. After experimenting with different bacteria such as pseudomonas aeruginosa, a bacterial found in soil, and citrobacter freundii and escherichia coli, bacteria found in humans, the white blood cells attacked and killed both. The reason he found this interesting he said, was because alligators' immune systems fought off bacteria, viruses and fungi they had never been exposed to. Another remarkable discovery he said, was that the cells also killed bacteria called candida albicans, yeast infections, and Methicillin-resistant Staphylococcus aureus (MRSA), staff infections, which claim numerous lives every year. He stated since humans are dying from these infections and alligator white blood cells are killing them, then they might be able to develop antibacterial, anti-viral or anti-fungal drugs for human medicine. "The way we think it works is that the outer coat of bacteria gives off a negative charge and the white blood cells give off a positive charge," he said. "So when opposites attract, the cells tear a hole in the membrane and therefore kills the bacteria." Merchant said his is really excited now that his research team has isolated these proteins and have determined their structure and now are trying to synthesize them. Students at LHS were surprised by a certain visitor Merchant brought with him; a four-year-old alligator. As the students exited the auditorium, they had the opportunity to touch and feel the texture of the alligator. Donell Evans, head of science department at LHS, said by having Merchant speak with the students, they hope to help them understand what's being offered outside of high school in terms of science related jobs and careers. Also, they are trying to bring more awareness to the Science, Technology, Engineer and Mathematics (STEM) programs that were recently introduced to Vernon Parish. The students in her AP biology class were so captivated with Merchant's research that they asked to discuss it more in depth during Friday's class. "I just think having a Louisiana college like McNeese State University being on the forefront with new antibiotics is amazing," Evans said. Merchant's researched has been funded by several grants including a four-year Research Competitiveness Subprogram grant from the Louisiana Board of Regents, EPSCoR travel grants to speak at five national and international conferences, EPSCoR Links with Industry and National Labs (LINK) grant to travel to Argentina as well as most recently, a grant from National Geographic.

Continued here:
Alligator cells prevail possible human medicine

Published: March 21, 2012

The Gairdner Foundation has announced the recipients of the 2012 Canada Gairdner Awards. Recognized for some of the most significant medical discoveries from around the world, this years winners showcase a broad range of new medical insights, from pioneering new ways to tackle childhood illness in developing countries to identifying how our biological clocks guide our everyday lives.

Among the worlds most esteemed medical research prizes, the awards distinguish Canada as a leader in science and provide a $100,000 prize to scientists whose work holds important potential. The 2012 winners are as follows:

Thomas M. Jessell, Ph.D.

Thomas M. Jessell, Ph.D., Howard Hughes Medical Institute, Kavli Institute for Brain Science, Columbia University Medical Center, New York, NY

The challenge: Through communication between the sensory neuron and the motor neuron in our bodies nervous system, we acquire the ability to move and react to the world around us. But little was known about how these neurons communicate with each other.

The work: Dr. Jessells work reveals the basic principles of nervous system communication. By studying the assembly and organization of the circuit that controls movement in the spinal cord nervous system, Dr. Jessell identified the direct connection between the sensory neuron, which is responsible for allowing us to process what is happening in the world around us, and the motor neuron, which allows us to control how our muscles move to react to what we sense in that world.

Why it matters: As a result of this discovery, we have the potential to create interventional strategies to treat and cure neurodegenerative diseases such as Amyotrophic Lateral Sclerosis (ALS) and Spinal Muscular Atrophy (SMA), where a problem with the circuit connection between the sensory neuron and the motor neuron prevents our minds and bodies from reacting properly to what we sense around us. Similarly, we now have the potential to restore movement in patients with spinal cord injury or paralysis.

(To learn more about Dr. Jessell and his work, read The Promise of the Brain.)

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Thomas Jessell Receives 2012 Gairdner Award for Groundbreaking Insights on Nervous System

Public release date: 19-Mar-2012 [ | E-mail | Share ]

Contact: Diana Yates diya@illinois.edu 217-333-5802 University of Illinois at Urbana-Champaign

CHAMPAIGN, lll. A new study describes how bacteria use a previously unknown means to defeat an antibiotic. The researchers found that the bacteria have modified a common "housekeeping" enzyme in a way that enables the enzyme to recognize and disarm the antibiotic.

The study appears in the Proceedings of the National Academy of Sciences.

Bacteria often engage in chemical warfare with one another, and many antibiotics used in medicine are modeled on the weapons they produce. But microbes also must protect themselves from their own toxins. The defenses they employ for protection can be acquired by other species, leading to antibiotic resistance.

The researchers focused on an enzyme, known as MccF, that they knew could disable a potent "Trojan horse" antibiotic that sneaks into cells disguised as a tasty protein meal. The bacterial antibiotic, called microcin C7 (McC7) is similar to a class of drugs used to treat bacterial infections of the skin.

"How Trojan horse antibiotics work is that the antibiotic portion is coupled to something that's fairly innocuous in this case it's a peptide," said University of Illinois biochemistry professor Satish Nair, who led the study. "So susceptible bacteria see this peptide, think of it as food and internalize it."

The meal comes at a price, however: Once the bacterial enzymes chew up the amino acid disguise, the liberated antibiotic is free to attack a key component of protein synthesis in the bacterium, Nair said.

"That is why the organisms that make this thing have to protect themselves," he said.

In previous studies, researchers had found the genes that protect some bacteria from this class of antibiotic toxins, but they didn't know how they worked. These genes code for peptidases, which normally chew up proteins (polypeptides) and lack the ability to recognize anything else.

Originally posted here:
Team discovers how bacteria resist a 'Trojan horse' antibiotic

The study appears in the Proceedings of the National Academy of Sciences.

Bacteria often engage in chemical warfare with one another, and many antibiotics used in medicine are modeled on the weapons they produce. But microbes also must protect themselves from their own toxins. The defenses they employ for protection can be acquired by other species, leading to antibiotic resistance.

The researchers focused on an enzyme, known as MccF, that they knew could disable a potent "Trojan horse" antibiotic that sneaks into cells disguised as a tasty protein meal. The bacterial antibiotic, called microcin C7 (McC7) is similar to a class of drugs used to treat bacterial infections of the skin.

"How Trojan horse antibiotics work is that the antibiotic portion is coupled to something that's fairly innocuous in this case it's a peptide," said University of Illinois biochemistry professor Satish Nair, who led the study. "So susceptible bacteria see this peptide, think of it as food and internalize it."

The meal comes at a price, however: Once the bacterial enzymes chew up the amino acid disguise, the liberated antibiotic is free to attack a key component of protein synthesis in the bacterium, Nair said.

"That is why the organisms that make this thing have to protect themselves," he said.

In previous studies, researchers had found the genes that protect some bacteria from this class of antibiotic toxins, but they didn't know how they worked. These genes code for peptidases, which normally chew up proteins (polypeptides) and lack the ability to recognize anything else.

Before the new study, "it wasn't clear how a peptidase could destroy an antibiotic," Nair said.

To get a fuller picture of the structure of the peptidase, Illinois graduate student Vinayak Agarwal crystallized MccF while it was bound to other molecules, including the antibiotic. An analysis of the structure and its interaction with the antibiotic revealed that MccF looked a lot like other enzymes in its family, but with a twist or, rather, a loop. Somehow MccF has picked up an additional loop of amino acids that it uses to recognize the antibiotic, rendering it ineffective.

"Now we know that specific amino acid residues in this loop are responsible for making this from a normal housekeeping gene into something that's capable of degrading this class of antibiotics," Nair said.

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Study finds how bacteria resist a 'Trojan horse' antibiotic

To Bob Rose and his colleagues, evolution isn't just a theoryit's the basis for their whole career.

"The idea of evolution is seminal to biochemistry," Rose, professor of biochemistry, said. Rose is currently working with the University, researching the gene that promotes insulin-production in various species.

"We do a lot of comparisons between species, which is very evolution-based." Rose said.

Rose is currently working on comparing the insulin promoter between humans, rats and mice in order to understand what things are conserved between the species. One of the key differences between these species is that mice have two insulin genes, whereas humans only have one.

"For some reason, the function was important enough to warrant two genes we see variations like that a lot," Rose said.

Despite those differences, enough is conserved between the proteins that regulate the genes and even the genes themselves that researchers can examine them as an important evolutionarily-preserved function.

According to Paul Wollenzien, professor of biochemistry, the first signs of evolution came at the earliest stages of life. Originally, polymers of RNA, nucleic acids that can code genetic information, self-competed for replication. Next came proteins translated from that primary genetic code, and finally life began to emerge.

Even in modern organisms, there are clues to these early events. For example, there are sequences within ribosomal RNA that are shared between the three domains of life: eukaryotes, prokaryotes and achaea. This means that the sequences were present within the progenitor of these domainsa common ancestor.

"Because we can recognize these universally-conserved sequences, we take that to mean that they were established early on in evolution," Wollenzien said. Because the sequences were established very early on, it indicates a great importance for the basic functions of life.

Evolution influences the emerging field of biochemistry with something called "Instant Evolution."

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Darwin peering through the molecular level

BELLINGHAM - Scientific measurements of the biochemistry of Lake Whatcom showed some improvement in 2011, but that is probably the result of a cool summer, not human efforts to control polluting runoff.

So says Robin Matthews, the lead scientist on the annual lake water monitoring effort commissioned by the city. Matthews is director of the Institute for Watershed Studies at Huxley College of the Environment, Western Washington University.

"I think we got a break last summer," Matthews said.

Cold and cloudy conditions kept water temperatures lower, and that delayed and diminished the annual explosion of algae populations that have affected lake quality in previous summers.

In the hotter summer of 2009, the algae concentrations got so high that they caused a serious cut in the capacity of the city's water treatment plant, resulting in mandatory water use restrictions. But even in a cool year like 2011, the algae growth was still enough to reduce the system's capacity, Matthews said.

While the scientific measurements taken in 2011 did show a reduction in levels of phosphorus and algae, Matthews said she believes the reductions were minor, and the summer's lower temperatures probably account for those reductions.

"It (pollution measurement) is down a little but it's not down much," Matthews said. "It doesn't show an improvement from watershed changes."

Matthews refuses to draw conclusions from any single year's worth of lake water measurements. Instead, she points to the whole series of measurements going back to 1994. Those measurements show year-to-year fluctuations, but a general rising trend in both phosphorus concentrations and algae growth.

As Matthews explained it, the lake's problems stem from phosphorus-laden runoff that is made worse by human activities in the watershed. The phosphorus nourishes algae growth, and the dead algae become food for bacteria. The bacteria, in turn, deplete dissolved oxygen and make the lake less hospitable to fish.

And it becomes a vicious circle, because the lower oxygen levels result in chemical changes that release additional phosphorus from compounds and make it usable for algae food.

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Cool 2011 summer helped Lake Whatcom water quality a bit

Public release date: 14-Mar-2012 [ | E-mail | Share ]

Contact: Clea Desjardins clea.desjardins@concordia.ca 514-848-2424 x5068 Concordia University

This press release is available in French.

Montreal -- Canada defines itself as a nation that stretches from coast to coast to coast. But can we keep those coasts healthy in the face of climate change? Yves Glinas, associate professor in Concordia's Department of Chemistry and Biochemistry, has found the solution in a surprising element: iron.

In a study published in Nature, Glinas along with Concordia PhD candidate Karine Lalonde and graduate Alexandre Ouellet, as well as McGill colleague Alfonso Mucci studies the chemical makeup of sediment samples from around the world ocean to show how iron oxides remove carbon dioxide from our atmosphere.

"People around the planet are fighting to reduce the amount of CO2 pumped into the atmosphere in the hopes of reducing climate change. But when it comes to getting rid of the CO2 that's already there, nature herself plays an important role," Glinas explains. CO2 is removed from the atmosphere and safely trapped on the ocean floor through a natural reaction that fixes the molecule to organic carbon on the surface of large bodies of water.

How exactly does that fixation process work? "For well over a decade, the scientific community has held onto the hypothesis that tiny clay minerals were responsible for preserving that specific fraction of organic carbon once it had sunk to the seabed," explains Mucci, whose related research was picked as one of the top 10 Scientific Discoveries of the year by Qubec Science. Through careful analysis of sediments from all over the world, Glinas and his team found that iron oxides were in fact responsible for trapping one fifth of all the organic carbon deposited on the ocean floor.

With this new knowledge comes increased concern: iron oxides are turning into what might be termed endangered molecules. As their name suggests, iron oxides can only form in the presence of oxygen, meaning that a well-oxygenated coastal ecosystem is necessary for the iron oxides to do their work in helping to remove carbon dioxide from the atmosphere. But there has been a worrying decrease in dissolved oxygen concentrations found in certain coastal environments and this trend is expanding. Locations once teeming with life are slowly becoming what are known as "dead zones" in which oxygen levels in the surface sediment are becoming increasingly depleted. That familiar culprit, man-made pollution, is behind the change.

Major rivers regularly discharge pollutants from agricultural fertilizers and human waste directly into lake and coastal environments, leading to a greater abundance of plankton. These living organisms are killed off at a greater rate and more organic carbon is sinking to the bottom waters, causing even greater consumption of dissolved oxygen. This makes the problem of low dissolved oxygen levels even worse. If the amount of oxygen in an aquatic environment decreases beyond a certain point, iron oxides stop being produced, thus robbing that environment of a large fraction of its natural ability to extract carbon dioxide from the atmosphere.

But there is hope. "This study also represents an indirect plea towards reducing the quantities of fertilizers and other nutrient-rich contaminants discharged in aquatic systems" explains Lalonde, who Glinas credits with much of the work behind this elemental study. She hopes that better understanding the iron-organic carbon stabilizing mechanism could "eventually lead to new ways of increasing the rate of organic carbon burial in sediments."

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Fielding questions about climate change

UTHSCT researchers receive five seed grants totaling $115,000

Five seed grants totaling $115,000 have been awarded to researchers at The University of Texas Health Science Center at Tyler. The locally raised money will help UTHSCT researchers explore new cures for serious diseases, saidSteven Idell, MD, Ph.D., UTHSCTs vice president for research.

Hong-Long Ji, Ph.D., associate professor of biochemistry, was awarded a $40,000 grant to study the relationship between abnormal genes and chronic obstructive pulmonary disease (COPD).

Usha Pendurthi, Ph.D., professor of molecular biology, received $40,000 to fund her work into how certain proteins that curb blood clotting affect the growth of cancerous tumors.

Proteins are required for the structure, function, and regulation of the bodys cells, tissues, and organs; each protein has unique functions. Hormones, enzymes, and antibodies are all examples of proteins.

Buka Samten, Ph.D., associate professor of microbiology and immunology, and Malini Madiraju, Ph.D., professor of biochemistry, were awarded $20,000 for preliminary research that could lead to a better vaccine against tuberculosis. Thats important, because TB kills more than a million people each year, according to the World Health Organization.

Anna Kurdowska, Ph.D., professor of biochemistry, received $10,000 for her research into a new way to treat acute lung injury, also known as acute respiratory distress syndrome (ARDS). And Amir Shams, Ph.D., associate professor of microbiology and immunology, received $5,000 to examine how to keep treatments for injured lungs inside those lungs.

These grants enable our scientists to pursue new and exciting research that could change our understanding of how serious diseases develop, as well as transform how we treat them. They help our researchers acquire the preliminary data they need to successfully compete for funding from the National Institutes of Health, the gold standard in biomedical research, Dr. Idell said, calling this years projects outstanding.

Funding for the seed grants comes from UTHSCs Research Council and the Texas Lung Injury Institute. Since 2002, scientists in the Center for Biomedical Research have been awarded $118.6 million in research dollars.

Continued here:
UTHSCT researchers receive five seed grants totaling $115,000

DUBLIN--(BUSINESS WIRE)--

Research and Markets (http://www.researchandmarkets.com/research/b561c1/biochemistry_for_s) has announced the addition of John Wiley and Sons Ltd's new book "Biochemistry for Sport and Exercise Metabolism" to their offering.

How do our muscles produce energy for exercise and what are the underlying biochemical principles involved? These are questions that students need to be able to answer when studying for a number of sport related degrees. This can prove to be a difficult task for those with a relatively limited scientific background. Biochemistry for Sport and Exercise Metabolism addresses this problem by placing the primary emphasis on sport, and describing the relevant biochemistry within this context.

The book opens with some basic information on the subject, including an overview of energy metabolism, some key aspects of skeletal muscle structure and function, and some simple biochemical concepts. It continues by looking at the three macromolecules which provide energy and structure to skeletal muscle - carbohydrates, lipids, and protein. The last section moves beyond biochemistry to examine key aspects of metabolism - the regulation of energy production and storage. Beginning with a chapter on basic principles of regulation of metabolism it continues by exploring how metabolism is influenced during high-intensity, prolonged, and intermittent exercise by intensity, duration, and nutrition.

Key Features:

Biochemistry for Sport and Exercise Metabolism will prove invaluable to students across a range of sport-related courses, who need to get to grips with how exercise mode, intensity, duration, training status and nutritional status can all affect the regulation of energy producing pathways and, more important, apply this understanding to develop training and nutrition programmes to maximise athletic performance.

Key Topics Covered:

For more information visit http://www.researchandmarkets.com/research/b561c1/biochemistry_for_s

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Research and Markets: Biochemistry for Sport and Exercise Metabolism

LOS ANGELES Researchers at the UCLA stem cell center and the departments of chemistry and biochemistry and pathology and laboratory medicine have identified, for the first time, a generic way to correct mutations in human mitochondrial DNA by targeting corrective RNAs, a finding with implications for treating a host of mitochondrial diseases.

Mutations in the human mitochondrial genome are implicated in neuromuscular diseases, metabolic defects and aging. There currently are no methods to successfully repair or compensate for these mutations, said study co-senior author Dr. Michael Teitell, a professor of pathology and laboratory medicine and a researcher with the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA.

Between 1,000 and 4,000 children per year in the United States are born with a mitochondrial disease and up to one in 4,000 children in the U.S. will develop a mitochondrial disease by the age of 10, according to Mito Action, a nonprofit organization supporting research into mitochondrial diseases. In adults, many diseases of aging have been associated with defects of mitochondrial function, including diabetes, Parkinson's disease, heart disease, stroke, Alzheimer's disease and cancer.

"I think this is a finding that could change the field," Teitell said. "We've been looking to do this for a long time and we had a very reasoned approach, but some key steps were missing. Now we have developed this method and the next step is to show that what we can do in human cell lines with mutant mitochondria can translate into animal models and, ultimately, into humans."

The study appears today in the peer-reviewed journal Proceedings of the National Academy of Sciences.

The current study builds on previous work published in 2010 in the peer-reviewed journal Cell, in which Teitell, Carla Koehler, a professor of chemistry and biochemistry and a Broad stem cell research center scientist, and their team uncovered a role for an essential protein that acts to shuttle RNA into the mitochondria, the energy-producing "power plant" of a cell.

Mitochondria are described as cellular power plants because they generate most of the energy supply within a cell. In addition to supplying energy, mitochondria also are involved in a broad range of other cellular processes including signaling, differentiation, death, control of the cell cycle and growth.

The import of nucleus-encoded small RNAs into mitochondria is essential for the replication, transcription and translation of the mitochondrial genome, but the mechanisms that deliver RNA into mitochondria have remained poorly understood.

The study in Cell outlined a new role for a protein called polynucleotide phosphorylase (PNPASE) in regulating the import of RNA into mitochondria. Reducing the expression or output of PNPASE decreased RNA import, which impaired the processing of mitochondrial genome-encoded RNAs. Reduced RNA processing inhibited the translation of proteins required to maintain the mitochondrial electron transport chain that consumes oxygen during cell respiration to produce energy. With reduced PNPASE, unprocessed mitochondrial-encoded RNAs accumulated, protein translation was inhibited and energy production was compromised, leading to stalled cell growth.

The findings from the current study provide a form of gene therapy for mitochondria by compensating for mutations that cause a wide range of diseases, said study co-senior author Koehler.

Link:
Repairing mutations in human mitochondria

The University of Texas Health Science Center at Tyler:

TYLER (KYTX) - Five seed grants totaling $115,000 have been awarded to researchers at The University of Texas Health Science Center at Tyler. The locally raised money will help UTHSCT researchers explore new cures for serious diseases, said Steven Idell, MD, Ph.D., UTHSCT's vice president for research.

Hong-Long Ji, Ph.D., associate professor of biochemistry, was awarded a $40,000 grant to study the relationship between abnormal genes and chronic obstructive pulmonary disease (COPD). Usha Pendurthi, Ph.D., professor of molecular biology, received $40,000 to fund her work into how certain proteins that curb blood clotting affect the growth of cancerous tumors.

Proteins are required for the structure, function, and regulation of the body's cells, tissues, and organs; each protein has unique functions. Hormones, enzymes, and antibodies are all examples of proteins.

Buka Samten, Ph.D., associate professor of microbiology and immunology, and Malini Madiraju, Ph.D., professor of biochemistry, were awarded $20,000 for preliminary research that could lead to a better vaccine against tuberculosis. That's important, because TB kills more than a million people each year, according to the World Health Organization.

Anna Kurdowska, Ph.D., professor of biochemistry, received $10,000 for her research into a new way to treat acute lung injury, also known as acute respiratory distress syndrome (ARDS). And Amir Shams, Ph.D., associate professor of microbiology and immunology, received $5,000 to examine how to keep treatments for injured lungs inside those lungs.

"These grants enable our scientists to pursue new and exciting research that could change our understanding of how serious diseases develop, as well as transform how we treat them. They help our researchers acquire the preliminary data they need to successfully compete for funding from the National Institutes of Health, the gold standard in biomedical research," Dr. Idell said, calling this year's projects "outstanding."

Funding for the seed grants comes from UTHSC's Research Council and the Texas Lung Injury Institute. Since 2002, scientists in the Center for Biomedical Research have been awarded $118.6 million in research dollars.

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Five seed grants totaling $115,000 awarded to UTHSCT researchers

We bring you a guest post today from Faraz Hussain, who studies biochemistry at Illinois Institute of Technology. Faraz is a student of Joseph Orgel, the biologist researching preserved dinosaur tissue whom we profiled in the latest episode of Clever Apes. Here, Faraz introduces us to a completely different way of bridging the eons to bring dinosaurs into the present day. Gabriel Spitzer

Dinosaurs 180 million-odd year reign may be considered a lively old romp by most, but some clever apes would prefer to study these fossils in the flesh. One particular suborder, the theropods, never really went extinct at all. The birds that descended from them are the nearest living relatives today of both raptors and tyrannosaursperhaps none more so than the humble hen. Paleontologist Jack Horner, one of the most vocal exponents of avian dinosaurs being all around us, would rather that hens' more imposing ancestors had not evolutionarily "chickened out" in the first place.

Instead of messing about with amber-encased mosquitoes gorged on dino-DNA and playing fill-in-the-blanks with frog and bird genomes la Jurassic Park, Horner has been rallying his paleontologist pals and evolutionary developmental biologists to try a fresh tack on resurrecting a dinosaur: He wants to reverse-engineer a chickenosaurus. Hey, why start from scratch when you already have a fully-formed dinosaur in need of just a few minor genetic modifications? What follows is not your grandma's stuffed chicken recipe:

Chicken fingers:

While birds may have opted for wings instead of claws, both the T. rex and the chicken have only three digits at the end of each. In birds, however, these fingers have fused together. Hans Larsson at McGill University's Redpath Museum is looking for ways to short-circuit the genetic pathway responsible for this process in the chicken's embryonic stage and allowing the digits to separate so that, instead of those delicious wings, it ends up with far deadlier talons instead.

Rump:

A chicken has only a handful of vertebrae at the end of its spine that fuse to form what passes for its tail. In 2007, Larsson observed a tail in a developing chick embryo that had 16, although by the time it hatched these had dwindled to five. Turn off the genetic mechanism that triggers the breakdown and absorption of the tail, and voilyou're well on your way to the 40 or so vertebrae found in some of the heftiest hindquarters ever: the T. rex tail.

Teeth:

Matthew Harris discovered the rudiments of teeth on a frankenchicken embryo called the talpid2 usually known for its polydactyl fingers. While a far cry from the toothy old tyrannosaur grin that we know and lovethe genome of a chicken doesnt contain genes coding for enamel, nor can they produce dentin, which made up the bulk of those formidable fangsits finally a fighting chance for poultry to bite back!

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Clever Apes: Cooking up a dino-chicken

Renowned Scientist receives IRL Industry and Outreach Fellowship

IRL has appointed Professor Juliet Gerrard, a biochemist and leader in the industrial application of biochemistry in New Zealand as its second Industry and Outreach Fellow.

IRLs Industry and Outreach Fellowships have been established as part of IRLs drive to strengthen links between the research and high-value manufacturing organisations.

New Zealands economic success depends on our ability to get greater coordination and alignment across our research and industry sectors. One area of significant potential is through greater mobility of highly talented people, says Shaun Coffey, IRL Chief Executive.

The Industry and Outreach Fellowships attract leaders from the research sector into IRL to develop areas of scientific research and assist with their application to industry.

Professor Gerrard, who runs the Biomolecular Interaction Centre at the University of Canterbury, has held a number of significant positions in recognition of her scientific work and has recently been appointed Chair of the Marsden Council.

Professor Gerrard sees the overall strategic aim of the Industry and Outreach Fellowship programme as boosting collaboration.

"There is a lot of research being done in both universities and industry and Id like to bridge that gap between fundamental and applied work," she says. "By collaborating with IRL I believe that we will be able to achieve this."

Professor Gerards track record includes stints working for Crop and Food Research Ltd, and conducting research for the likes of Fonterra. She is also a principal investigator at the MacDiarmid Institute and Riddet Institute and has been on a number of editorial boards for scientific journals. She has written over 100 journal articles.

IRL Industry and Outreach Fellows are initially appointed for a five-year term and are mandated to resolve industry-related problems while building links between research institutions and business.

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Renowned Scientist receives IRL Industry and Outreach Fellow