UCSB Professors Receive National Chemistry Awards

Two UC Santa Barbara professors have been named recipients of the American Chemical Societys 2013 national awards for professionaladvancement. Peter C. Ford, professor in the Department of Chemistry and Biochemistry, and Craig J. Hawker, also a professor in the Department of chemistry and Biochemistry,professor of materials, and director of the Materials Research Laboratory, have been named among the 64 award winners from across the country

In only one other year, 1996, did UCSB have more than one winner of theAmerican Chemical Society (ACS) awards. The awards will be presented at the nationalACS meeting in New Orleans in April.Ford is the recipient of the ACS Award for Distinguished Service in the Advancement of Inorganic Chemistry. This award recognizes individuals who haveadvanced inorganic chemistry by significant service, in addition to performingoutstanding research. It is sponsored by StremChemicals.

I am of course very pleased and honored to have received this award from my colleagues in the American Chemical Society, saidFord.

Since this is largely in recognition of the body of work generated by my graduate and postdoctoral students and collaborators over my tenure at UCSB, I consider it an award to my research group collectively as well as another testament to the high regard in which this campus is nowheld. I am proud to be aGaucho.

Hawker has been named recipient of the ACS Award in Polymer Chemistry. Thecitation states that Hawker was nominated for transforming the field of polymer chemistry through the clever adaptation of synthetic organic chemistry concepts and theadvancement of macromolecular engineering. ExxonMobil Chemical Company sponsored thisaward.

I am thrilled with the award and the recognition that it brings to my students, collaborators, and co-workers, as well as to the unique research environment at UCSB, said Hawker. The sustained success of cross-disciplinary research has been a key driver in reinforcing UCSBs international standing in the materials chemistry arena. I am grateful for the enormous benefits that this proud tradition has bought to myresearch.

Ford joined the faculty at UCSB in 1967 after earning his Ph.D. at Yale and completing a National Science Foundation postdoctoral fellowship with Nobel laureateHenry Taube at Stanford University. He is a Fellow of the American Association for theAdvancement of Science and was a Senior Fulbright Fellow. His awards include a Dreyfus Foundation Teacher-Scholar Award in 1972; the Alexander von Humboldt Foundation Senior U.S. Scientist Award in 1992; the Richard C. Tolman Medal of theACS in 1993; and the Inter-American Photochemical Society Award in Photochemistry in2008.

Hawker received his Ph.D. from the University of Cambridge, and then completeda postdoctoral fellowship with Jean M. J. Frchet at Cornell. In 2004, he moved from theIBM Almaden Research Center to join the faculty at UCSB. Some of his recent awardsinclude the 2012 Centenary prize from the Royal Society of Chemistry; the 2011 Arthur C. Cope Scholar from the American Chemical Society; and the 2008 DSM PerformanceMaterials Award from the International Union of Pure and Applied Chemistry. In 2010,he was named a Fellow of the RoyalSociety.

Here is the original post:
UCSB Professors Receive National Chemistry Awards

Study Shows Optiferrin™ Recombinant Human Transferrin Is Comparable to Serum-Derived or Mammalian-Expressed Transferrin

FORT COLLINS, Colo.--(BUSINESS WIRE)--

Optiferrin, a recombinant human transferrin (rhTF) protein produced by Ventria Bioscience using ExpressTec, has been shown to be biochemically and structurally similar to human transferrin (hTF) molecules derived either from human serum or a recombinant mammalian expression system, according to a paper published today in the Journal of Inorganic Biochemistry.1 Optiferrin is sold commercially by InVitria, the bioreagents division of Ventria Bioscience, for use in cell culture applications.

Recombinant human transferrin used in cell culture media supplements is available from a number of commercial sources, but characterization of these products rarely goes beyond a crude assessment of purity by gel electrophoresis, said Dr. Anne B. Mason, Research Professor of Biochemistry at the University of Vermont (Burlington, Vt.) and the senior author on the study. Functional validation by more thorough and quantitative methods such as ours is essential for either analytical purposes or for pharmaceutical development.

The paper, titled Biochemical and Structural Characterization of Recombinant Human Serum Transferrin from Rice (Oryza sativa L.), was the result of a collaboration between researchers at the University of Vermont College of Medicines Department of Biochemistry; the University of Massachusetts at Amhersts Department of Chemistry, (Amherst, Mass.); Ventria Bioscience; and InVitria. The research team used a battery of biochemical and biophysical techniques to compare the functional properties of Optiferrin to either native hTF purified from human serum, or a reference form of recombinant N-His-tagged nonglycosylated human transferrin (referred to as N-His hTF). As authorities on the biochemical properties of proteins involved in iron metabolism, Dr. Masons group had previously developed and characterized the mammalian expression system used to produce the N-His hTF protein and mutant variations and also developed many of the biophysical techniques used in this study as part of their ongoing research.

The in-depth biochemical and structural characterization analysis included techniques such as peptide mapping and capillary liquid chromatography with tandem mass spectrometry; circular dichroism spectrometry; ultraviolet-visible (UV-vis) spectroscopy; determination of molar absorption coefficient for iron; steady-state tryptophan fluorescence; relative transferrin-receptor binding affinity; and iron release under simulated endosomal conditions. The results demonstrated that Optiferrin is biochemically and structurally similar to hTF, exhibiting the tight but reversible binding to iron (Fe3+) that is a hallmark of transferrin function.

Human transferrin, either purified from human blood serum or biomanufactured using various recombinant protein expression systems, is widely used in biomedical research and the biotechnology industry as a supplement to support mammalian cell growth in serum-free cell culture media. It also has potential therapeutic uses in the treatment of thalassemia, atransferrinemia, and age-related macular degeneration, and as an anti-cancer drug delivery molecule. However, hTF sourced from serum poses the risk of transmission of blood-borne pathogens, while current systems for recombinant expression are difficult to scale in a cost-effective manner for biopharmaceutical applications. Thus a cost-efficient production method is desirable. The authors of the present study performed a basic economic analysis of current rhTF biomanufacturing methods (Table S1) and found that rhTF produced using Ventria Biosciences ExpressTec technology is dramatically more cost effective than other commercial methods, including yeast, immortalized human cell lines (HEK293), or wheat germ.

While we have long known that Optiferrin supports optimal cell growth in serum-free media, this study provides further validation that recombinant human transferrin produced using our ExpressTec technology functions similarly to its endogenous counterpart, said Scott Deeter, president and CEO of Ventria Bioscience. These results will support our future efforts toward developing a cost-effective, biopharmaceutical-grade human transferrin product.

1 Full citation: Steere AN, Bobst CE, Zhang D, Pettit S, Kaltashov IA, Huang N, Mason AB. Biochemical and structural characterization of recombinant human serum transferrin from rice (Oryza sativa L.). J Inorg Biochem. 2012;116:37-44. doi: 10.1016/j.jinorgbio.2012.07.005.

About InVitria

InVitria develops, manufactures and markets a portfolio of animal-free cell culture supplements that improve performance, cost effectiveness and consistency of cell-based biomanufacturing systems. InVitria is a division of Ventria Bioscience. For more information, visit http://www.invitria.com.

The rest is here:
Study Shows Optiferrin™ Recombinant Human Transferrin Is Comparable to Serum-Derived or Mammalian-Expressed Transferrin

Newly discovered molecule could deliver drugs to treat diseases

Public release date: 24-Sep-2012 [ | E-mail | Share ]

Contact: John Tomich jtomich@k-state.edu 785-532-5956 Kansas State University

MANHATTAN, Kan. -- Kansas State University researchers have discovered a molecule that may be capable of delivering drugs inside the body to treat diseases.

For the first time, researchers have designed and created a membrane-bounded vesicle formed entirely of peptides -- molecules made up of amino acids, the building blocks of protein. The membrane could serve as a new drug delivery system to safely treat cancer and neurodegenerative diseases.

A study led by John Tomich, professor of biochemistry at Kansas State University, has been published in the journal PLOS ONE in September, and a patent for the discovery is pending.

The peptides are a set of self-assembling branched molecules made up of naturally occurring amino acids. The chemical properties of a peptide create a vesicle that Tomich describes as a bubble: It's made up of a thin membrane and is hollow inside. Created in a water solution, the bubble is filled with water rather than air.

The peptides -- or bubbles -- can be made in a solution containing a drug or other molecule that becomes encapsulated as the peptide assembles, yielding a trapped compound, much like a gelatin capsule holds over-the-counter oral remedies. The peptide vesicles could be delivered to appropriate cells in the body to treat diseases and minimize potential side effects.

"We see this as a new way to deliver any kind of molecule to cells," Tomich said. "We know that in certain diseases subpopulations of cells have gone awry, and we'd like to be able to specifically target them instead of attacking every cell, including healthy ones."

The finding could improve gene therapy, which has the potential to cure diseases by replacing diseased cells with healthy ones. Gene therapy is being tested in clinical trials, but the biggest challenge is how best to deliver the genes.

Methods include cells with a virus being injected into the body, and liposomes -- fatty compounds -- carrying the genes. However, these methods may present some problems.

Read the original here:
Newly discovered molecule could deliver drugs to treat diseases

Third Rock Ventures Launches MyoKardia with $38 Million to Address Genetic Heart Disease

SAN FRANCISCO & BOSTON--(BUSINESS WIRE)--

Third Rock Ventures, LLC today announced the formation of MyoKardia, Inc. with a $38 million Series A financing of the company. MyoKardia is developing a pipeline of novel small molecule therapeutics that address key clinical needs for patients with genetic heart disease. The companys first programs include hypertrophic and dilated cardiomyopathy, which together afflict approximately 1 million people in the United States, and for which no novel therapeutics have been brought to market in over a decade. MyoKardias proprietary drug discovery platform brings together advances from the fields of cardiovascular genomics and heart muscle biology to enable its scientists to target certain heart disease at its source. This genetically targeted approach has the potential to revolutionize the treatment of cardiomyopathies, and ultimately a broader spectrum of cardiovascular disease, including heart failure. The company is founded by world leaders in the fields of muscle biology and cardiovascular genetics: James Spudich, Ph.D., Professor of Biochemistry, Stanford University, Leslie Leinwand, Ph.D., Professor of Molecular, Cellular and Developmental Biology, University of Colorado, Christine Seidman, M.D., Professor of Medicine and Genetics, Harvard Medical School and Director of the Cardiovascular Genetics Center at Brigham and Womens Hospital, and Jonathan Seidman, Ph.D., Professor of Genetics, Harvard Medical School.

The last decade has been challenging for those pursuing novel therapeutics in the cardiovascular space, in part because most treatments target symptoms far downstream of the root cause, said Dr.Leinwand. MyoKardias approach addresses this challenge head on by employing genetics to more precisely define the disease and who we want to treat, and by employing cutting-edge muscle biochemistry and a novel platform to determine how we want to treat. Our initial targets are genetic cardiomyopathies, but this could very well be a novel and tractable therapeutic discovery approach to even larger diseases like heart failure.

Abnormalities in the basic unit of heart muscle, called the sarcomere, have been identified as the driving cause for a variety of heart disease, and the most common cause of hypertrophic and dilated cardiomyopathy. Mutations in the proteins of the sarcomere cause disease by rendering the muscle either hyper or hypo contractile. MyoKardias platform brings together recent assay and protein expression advances pioneered by its founders with genetic insights to enable a personalized medicine approach. This allows for the rapid development of mutation-specific sarcomeric allosteric modulators that rebalance contractility, therefore stopping and potentially reversing the course of disease. MyoKardias approach will leverage resident expertise in sarcomere genetics, in-vivo and in-vitro disease models, next-generation biochemical and biophysical assay development, and medicinal chemistry. Together, these capabilities will provide for the efficient progression of multiple programs in DCM, HCM, and other genetic cardiomyopathies and heart disease related to sarcomere dysfunction.

With MyoKardias platform, we have the ability to exquisitely characterize the biochemistry and biophysics of the human mutated sarcomere, said Dr. Spudich. This not only allows us to better understand what drives pathophysiology, it also points us toward potential mutant specific solutions.

Our goal is to provide treatments for patients with genetic diseases for whom the options to date have been profoundly limited, said Charles Homcy, M.D., interim chief executive officer of MyoKardia and venture partner at Third Rock Ventures. With this Series A financing, we can meet our goals. We now have the resources and capabilities to effectively translate the insights of our founders and employees into multiple clinical products that positively impact patient lives.

Hypertrophic and dilated cardiomyopathies, MyoKardias first two focus disease areas, are the most common forms of heart muscle disease and the most common diagnosis leading to cardiac transplantation. More than 60 million people worldwide have cardiomyopathy or carry a cardiomyopathy gene mutation, including approximately 1 million patients in the United States. Despite this large patient population and the persisting unmet clinical need, there is a lack of novel therapeutics being developed that directly target these diseases.

About Genetic Cardiomyopathy

Genetic cardiomyopathies are conditions that arise from mutation in a critical heart muscle protein. Hypertrophic cardiomyopathy (HCM) produces thickening of the heart walls and is best known as a leading cause of sudden cardiac death in young athletes. Dilated cardiomyopathy (DCM) produces weakening of the heart walls and enlargement of the heart chambers. Cardiomyopathy can occur at any age, and more than 30,000 children, from newborns to 18-year-olds, suffer from some form of cardiomyopathy in the United States a patient population comparable to the number of people living with cystic fibrosis.

About MyoKardia, Inc.

Follow this link:
Third Rock Ventures Launches MyoKardia with $38 Million to Address Genetic Heart Disease

Biochemistry: New technique to study interaction of metal ions in a liquid

In the heart of the LOI88 experiment: this is the point where the metal ions (from the left) enter the drop.

In August, the members of an ISOLDE project called LOI88 successfully employed a new technique to study the interaction of metal ions in a liquid. It's the first time that specific ions have been studied in a liquid medium - a technical achievement that opens promising doors for biochemistry.

"More than half of the proteins in the human body contain metal ions such as magnesium, zinc and copper," explains Monika Stachura, a biophysicist at the University of Copenhagen and the LOI88 project leader. "We know that these elements are crucial to a protein's structure and function but their behaviour and interactions are not known in detail." Detecting these ions directly in a body-like environment is problematic as their closed atomic shells make them invisible to most spectroscopic techniques. However, using the beta-Nuclear Magnetic Resonance (-NMR) technique in combination with the COLLAPS beamline the LOI88 team succeeded, for the first time, in recording a signal from metal ions in a body-like liquid environment. This also proves that basic nuclear physics research and techniques can lead to novel applications.

To obtain these excellent results, the team first had to meet a challenge: to find a way to introduce "easily visible" metal ions into a liquid, in order to then "see" their signal. And by "visible", ISOLDE physicists of course mean "radioactive". Their choice: radioactive magnesium 31 ions (31Mg++). The technique: -NMR. The setup: complicated

"First of all, we needed aMg31 ion beam from ISOLDE," says Magdalena Kowalska, a -NMR physicist participating in the project and the ISOLDE physics coordinator. "As we are using the NMR technique, we have to polarize the spins of these ions, which is done using laser light from the ISOLDE-COLLAPS set-up. The polarized ions are then caught by a drop of the liquid." Sounds easy? Not if you consider that the beam has to stay in a vacuum, but the liquid cannot. "When a liquid solution is placed in a vacuum it first boils and then freezes, making it impossible to perform the experiment," explains Alexander Gottberg, an ISOLDE target physicist from CSIC, Madrid, who designed the experimental set-up. "To overcome the problem, we had to introduce a pressure difference between the weak vacuum around the liquid target and the high vacuum in the beamline. The most challenging part of this design was that the differential pumping system, which was used for this purpose, had to be hosted on just a few centimeters."

Enlarge

A falling drop during the measurements.

But what does this anisotropy mean? "From our theoretical models, we can deduce the interactions of the metal ions in the liquid by looking at the NMR radiofrequency that cancels the anisotropy," explains Alexander.

"By proving the feasibility of the technique, we have opened new doors for biochemistry," concludes Monika. "We are now preparing the next steps: injecting macromolecules and later proteins into the liquid to see how metal ions interact with them." The three experts confided that they were "extremely excited". No kidding!

Provided by CERN

Read more here:
Biochemistry: New technique to study interaction of metal ions in a liquid

Purple corn compound may aid in developing future treatments for Type 2 diabetes, kidney disease

Public release date: 18-Sep-2012 [ | E-mail | Share ]

Contact: Donna Krupa dkrupa@the-aps.org American Physiological Society

BETHESDA, Md. (Sept. 18, 2012)Diabetic nephropathy is one of the most serious complications related to diabetes, often leading to end-stage kidney disease. Purple corn grown in Peru and Chile is a relative of blue corn, which is readily available in the U.S. The maize is rich in anthocyanins (also known as flavonoids), which are reported to have anti-diabetic properties. Scientists from the Department of Food and Nutrition and Department of Biochemistry at Hallym University in Korea investigated the cellular and molecular activity of purple corn anthocyanins (PCA) to determine whether and how it affects the development of diabetic nephropathy (DN). Their findings suggest that PCA inhibits multiple pathways involved in the development of DN, which may help in developing therapies aimed at type 2 diabetes and kidney disease.

The study is entitled "Purple corn anthocyanins inhibit diabetes-associated glomerular monocyte activation and macrophage infiltration" http://bit.ly/SlrkRY. It appears in the online edition of the American Journal of Physiology Renal Physiology, published by the American Physiological Society (APS; http://www.the-aps.org).

Methodology

Researcher Min-Kyung Kang and colleagues performed a two-part study, an in vitro experiment investigating the effects of PCA on human endothelial cells cultured under hyperglycemic kidney conditions and an in vivo study that investigated the effects of PCA on kidney tissue in diabetic mice. In the in vitro experiment, cultured cells were exposed to 1-20 g/ml of PCA for six hours (control cells were not exposed), then assessed for level of monocyte-endothelial cell adhesion, a major factor in the development of diabetic glomerulosclerosis. In the in vivo experiment, diabetic and control mice were dosed with PCA for eight weeks, then changes in kidney tissue were assessed and immunohistological analyses were performed. Kidney tissue was further analyzed for levels of inflammatory chemokines, which are key components in DN.

Results

Researchers found that in human endothelial cells cultured in hyperglycemic kidney conditions, induction of endothelial cell adhesion molecules decreased in a dose-dependent manner with PCA exposure, meaning that the PCA likely interfered with cell-cell adhesion in glomeruli. PCA also appeared to interfere with leukocyte recruitment and adhesion to glomerular endothelial cells. In diabetic mice, PCA exposure slowed mesangial expansion and interrupted the cellular signaling pathway that may instigate glomerular adhesion and infiltration of inflammatory cells responsible for diabetic glomerulosclerosis. Finally, PCA inhibited levels of macrophage inflammatory protein-2 and monocyte chemotactic protein-1 in kidney tissue, demonstrating that it may inhibit macrophage infiltration, which is closely related to renal inflammation.

Importance of the Findings

The research suggests that anthocyanins may be the main biofunctional compound in purple corn and could protect against mesangial activation of monocytes and infiltration of macrophages in glomerulithe two major contributors to DN. The research further suggests that renoprotection by PCA against mesangial activation may be specific therapies targeting diabetes-associated diabetic glomerulosclerosis and renal inflammation. Finally, PCA supplementation may be an important strategy in preventing renal vascular disease in type 2 diabetes.

Read the original here:
Purple corn compound may aid in developing future treatments for Type 2 diabetes, kidney disease

Compound found in purple corn may aid in developing future treatments for type 2 diabetes, kidney disease

ScienceDaily (Sep. 18, 2012) Diabetic nephropathy is one of the most serious complications related to diabetes, often leading to end-stage kidney disease. Purple corn grown in Peru and Chile is a relative of blue corn, which is readily available in the U.S. The maize is rich in anthocyanins (also known as flavonoids), which are reported to have anti-diabetic properties.

Scientists from the Department of Food and Nutrition and Department of Biochemistry at Hallym University in Korea investigated the cellular and molecular activity of purple corn anthocyanins (PCA) to determine whether and how it affects the development of diabetic nephropathy (DN). Their findings suggest that PCA inhibits multiple pathways involved in the development of DN, which may help in developing therapies aimed at type 2 diabetes and kidney disease.

The study is entitled "Purple corn anthocyanins inhibit diabetes-associated glomerular monocyte activation and macrophage infiltration." It appears in the online edition of the American Journal of Physiology -- Renal Physiology, published by the American Physiological Society.

Methodology

Researcher Min-Kyung Kang and colleagues performed a two-part study, an in vitro experiment investigating the effects of PCA on human endothelial cells cultured under hyperglycemic kidney conditions and an in vivo study that investigated the effects of PCA on kidney tissue in diabetic mice. In the in vitro experiment, cultured cells were exposed to 1-20 g/ml of PCA for six hours (control cells were not exposed), then assessed for level of monocyte-endothelial cell adhesion, a major factor in the development of diabetic glomerulosclerosis. In the in vivo experiment, diabetic and control mice were dosed with PCA for eight weeks, then changes in kidney tissue were assessed and immunohistological analyses were performed. Kidney tissue was further analyzed for levels of inflammatory chemokines, which are key components in DN.

Results

Researchers found that in human endothelial cells cultured in hyperglycemic kidney conditions, induction of endothelial cell adhesion molecules decreased in a dose-dependent manner with PCA exposure, meaning that the PCA likely interfered with cell-cell adhesion in glomeruli. PCA also appeared to interfere with leukocyte recruitment and adhesion to glomerular endothelial cells. In diabetic mice, PCA exposure slowed mesangial expansion and interrupted the cellular signaling pathway that may instigate glomerular adhesion and infiltration of inflammatory cells responsible for diabetic glomerulosclerosis. Finally, PCA inhibited levels of macrophage inflammatory protein-2 and monocyte chemotactic protein-1 in kidney tissue, demonstrating that it may inhibit macrophage infiltration, which is closely related to renal inflammation.

Importance of the Findings

The research suggests that anthocyanins may be the main biofunctional compound in purple corn and could protect against mesangial activation of monocytes and infiltration of macrophages in glomeruli -- the two major contributors to DN. The research further suggests that renoprotection by PCA against mesangial activation may be specific therapies targeting diabetes-associated diabetic glomerulosclerosis and renal inflammation. Finally, PCA supplementation may be an important strategy in preventing renal vascular disease in type 2 diabetes.

"PCA may be a potential renoprotective agent treating diabetes-associated glomerulosclerosis," wrote the researchers.

Go here to read the rest:
Compound found in purple corn may aid in developing future treatments for type 2 diabetes, kidney disease

Embryo-Critical Protein Modeled In 3D For First Time

Featured Article Academic Journal Main Category: Biology / Biochemistry Also Included In: Genetics;Cancer / Oncology Article Date: 18 Sep 2012 - 10:00 PDT

Current ratings for: Embryo-Critical Protein Modeled In 3D For First Time

Their findings are due to be published in a new journal called eLife, expected be launched this winter.

The team is led by biophysicist Eva Nogales, an electron microscopy expert with the US Department of Energy (DOE)'s Lawrence Berkeley National Laboratory (Berkeley Lab) in Berkeley, California, and one of two corresponding authors on the journal paper.

"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," says Nogales in a recent press statement.

For instance, mouse studies have shown deletion of any of its components either leads to death of the embryo or severe defects.

Scientists have also shown than PRC2 helps control differentiation of embryonic stem cells into other types of cell: the protein silences key genetic messages in the cell nucleus to effect this, as Nogales explains:

"PRC2 controls stem cell differentiation by regulating the expression of specific genes through the binding and methylation of histones, the proteins in chromatin that help bundle DNA into nucleosomes."

Such reasons are why the protein is what Nogales describes as one of the "top targets" for drug developers.

Nogales and colleagues produced their 3D model by painstakingly piecing together a jigsaw of data from many different sources, such as protein biochemistry, 3D electron microscopy, mass spectrometery, chemical cross-linking, and crystal structure docking.

Read the original here:
Embryo-Critical Protein Modeled In 3D For First Time

Wexford Online University Names Dr. Charles Foltz Professor with Focus on Science in Health and Fitness Field

Wexford Online University Names Dr. Charles Foltz Professor with Focus on Science in Health and Fitness Field

Dr. Charles Brown was recently named professor for Wexford University, where he will teach biochemistry, physiology and more with a focus on health and fitness. The 100 percent university offers a variety of health, exercise, sports and fitness degree programs of all levels to both U.S. and international students.

With a masters of Public Health in Epidemiology and doctorate in Interdisciplinary Molecular and Cellular Biology from Tulane University and a bachelors degree in Molecular Neuroscience from the University of California at Santa Barbara, Foltz is currently vice president of Research and Development at eHealth Screenings and senior project officer at Hip Hop Public Health. He is also the creator of 360 Cardio and has partnered with Polar heart rate monitors, the National Exercise and Sports Trainers Association (NESTA) and Total Health Interactive (THI). In addition, Foltz is a strength and conditioning coach and professional triathlon coach and manager. At Wexford University online, Foltz will teach subjects such as Biochemistry and Advanced Exercise Physiology with a focus on health and fitness for both local and international students.

Charles will offer Wexfords online students the perfect combination of science and real-world health and fitness experience and knowledge, said Jack Bauerle, Chancellor of Wexford University. He has worked with health and fitness organizations and individuals across the world, and were very pleased that hes bringing that wealth of wellness knowledge to Wexfords local and international students.

In addition, Foltz has earned certifications from the National Strength and Conditioning Association as a Certified Strength and Conditioning Coach and the National Academy of Sports Medicine as a Certified Performance Enhancement Specialist, a Certified Corrective Exercise Specialist and a Certified Personal Trainer.

Wexford University offers degree programs including an associate of arts degree in Fitness Training, a bachelor of science degree in Health and Fitness, a master of science degree in Nutrition and Exercise, a master of arts in Applied Sports Psychology and a doctorate degree in Applied Sports Psychology.

Wexford University is dedicated to providing world-class education through cutting-edge technology, offering direct application degree programs in an accelerated format with 100 percent online learning to save time and money. Programs include an associate of arts degree in Fitness Training, bachelors degree in Health and Fitness, masters degree in Nutrition and Exercise as well as masters degree and doctorate degree in Applied Sport Psychology. Wexford University is the higher education division of NESTA (National Exercise & Sports Trainers Association). For more information, please visit http://wexford.edu/.

See the original post:
Wexford Online University Names Dr. Charles Foltz Professor with Focus on Science in Health and Fitness Field

New gene could lead to better bug-resistant plants

ScienceDaily (Sep. 17, 2012) The discovery of a new gene could lead to better bug-resistant plants.

Research led by Michigan State University and appearing on the cover of this week's Proceedings of the National Academy of Sciences, demonstrates that domestic tomatoes could re-learn a thing or two from their wild cousins.

Long-term cultivation has led to tomato crops losing beneficial traits common to wild tomatoes. Anthony Schilmiller, MSU research assistant professor of biochemistry and molecular biology, was able to identify a gene that is involved in one of these beneficial traits.

Many tomato secrets are found in its hair. Trichomes, or hair-like protrusions, produce a mixture of specialized chemicals that shape the interactions between the plant and its environment. The location of the chemicals allows some of them to act as the first line of defense against pests.

One class of compounds, acyl sugars, is a frontline defender. Trichomes secrete acyl sugars to fend off pests. Schilmiller teamed with Robert Last, MSU professor of biochemistry and molecular biology, and Amanda Charbonneau, MSU doctoral researcher, to try to understand how these chemicals are made. Little was known about how acyl sugars were produced until now, and this research identifies and describes the first gene that participates in the production of the protective sugars in cultivated tomatoes, Schilmiller said.

"Acyl sugars play a critical role in allowing wild tomatoes to fend off bugs," he said. "Because cultivated tomatoes were not bred for their acyl sugar amounts and quality, they have reduced levels compared to wild ones we do not eat. Understanding how they are made is the first step toward breeding cultivated tomatoes, and other plants in this family, to make them more resistant to herbivores."

Other Solanaceous crops that could benefit from this research include potatoes, peppers, eggplants and petunias.

In addition, this work shows that the newly discovered gene is active only in one specific cell of one trichome type.

"Not only will we be able to potentially engineer heartier tomatoes, but understanding how to specifically target trichome gene expression without affecting the fruit, we'll also be able to add other important chemicals for insect resistance and possibly other beneficial traits to the surface of the plants," Schilmiller said.

The research was funded by the National Science Foundation.

Read the original post:
New gene could lead to better bug-resistant plants

Chemists develop reversible method of tagging proteins

ScienceDaily (Sep. 16, 2012) Chemists at UC San Diego have developed a method that for the first time provides scientists the ability to attach chemical probes onto proteins and subsequently remove them in a repeatable cycle.

Their achievement, detailed in a paper that appears online this week in the journal Nature Methods, will allow researchers to better understand the biochemistry of naturally formed proteins in order to create better antibiotics, anti-cancer drugs, biofuels, food crops and other natural products. It will also provide scientists with a new laboratory tool they can use to purify and track proteins in living cells.

The development was the culmination of a 10 year effort by researchers in the laboratory of Michael Burkart, a professor of chemistry and biochemistry, to establish a method to both attach a chemical probe at a specific location on a protein and selectively remove it. This flexibility allows researchers to study the protein with many different functional attachments, providing versatility akin to a biochemical Swiss Army knife. The great advantage of this technique is the broad flexibility of the attachments, which can be dyes, purification agents or mimics of natural metabolic products. Each of these attachments can be used for different purposes and biological studies.

Burkart's goal in his own laboratory is to understand more about the biochemical pathways of fatty acid metabolism and the biosynthesis of other natural products. One project focuses on engineering algae in order to produce improved biofuels. In this effort, the scientists hope to maximize the production of high quality algae oils, which could be used to supplement or supplant existing fossil fuels.

"In fatty acid metabolism, the fatty acids grow from an arm that eventually curls around and starts interacting with the metabolic protein," said Burkart, who is also associate director of the San Diego Center for Algae Biotechnology, or SD-CAB, a consortium of institutions in the San Diego region working together to make biofuels from algae commercially viable as transportation fuels. "What we wanted to know was how long does the growing fatty acid get before it starts binding with the protein?"

Burkart and chemists in his laboratory -- Nicolas Kosa, Robert Haushalter and Andrew Smith -- found a way to remove the chemical probe from this metabolic protein using an enzyme called a phosphodiesterase derived from the common bacterium Pseudomonas aeruginosa. Subsequent reattachment of a fatty acid analogue reconstituted the protein complex to its natural state. By repeating the process again and again, while examining the molecular changes in the fatty acid with nuclear magnetic spectroscopy, or NMR, during different metabolic stages, the scientists were able to detail the biochemical pathway of the fatty acid metabolism in a way they had never been able to do before.

"Without this tool, we would really have very limited ways of studying the dynamics of these fundamental metabolic processes," Burkart said. "This opened the door for us to finally examine in detail the fatty acid biosynthesis shared by algae, which you have to understand if you want to engineer ways to improve the quantity of oil that's made by algae or to make different types of oil molecules in algae that are better for biofuels."

The UC San Diego chemists also used NMR to verify that the process of chemically removing and attaching the chemical probes does not degrade or alter the protein in any way. "We've shown that we can do this iteratively, at least four or five times, without any degradation of the protein," said Burkart. "The protein remains very stable and can be studied very easily."

Because these same metabolic processes are shared by the metabolism of many natural products, including anti-cancer agents, antibiotics, and natural insecticides, Burkart said this new tool should have wide application in natural product chemistry labs.

"These are fundamental biochemical pathways that we still don't fully understand," he said. "We're now learning how these basic biosynthetic enzymes work. A large majority of drugs are derived from natural products and many future medicines can result from these pathways. There's a great interest now in synthetic biology, using these pathways to make new antibiotics or new anti-cancer drugs. They're all regulated by these same types of interactions."

Go here to read the rest:
Chemists develop reversible method of tagging proteins

Regents set to confirm executive director

Regents set to confirm executive director

Center for Teaching Excellence: a program whose goal is to assist faculty with implementing technology-driven course enhancements and advanced features of the electronic course management system.

Source: OU Public Affairs

A new director has been appointed to a program at OU designed to help faculty improve courses with new technology.

Teaching strategies expert Mark Morvant, a professor in the department of chemistry and biochemistry, will be appointed Oct. 1 as the executive director of the Center for Teaching Excellence, as long as the OU Board of Regents approves his appointment at its September meeting, according to an OU press release.

Morvant will work with Michele Eodice, associate provost for academic engagement, to embed writing strategies within disciplines across the campus and increase the use of other high-impact instructional techniques, according to the press release.

I think the future for the University of Oklahoma is very bright I think theres an excitement among the faculty about improving the educational experience for our students, and Im honored to lead our faculty in improving the students education, Morvant said.

In 2006, Morvant began teaching at OU as a chemistry professor and was named assistant chairman of the chemistry and biochemistry department in 2011, according to the press release.

He will step down from teaching for a few years to build the Center for Teaching Excellence program but plans on eventually returning to limited teaching on a routine basis, Morvant said.

Morvant also will be stepping down from his position as assistant chairman of the chemistry and biochemistry department but will continue to have a faculty appointment in the department, he said.

Continue reading here:
Regents set to confirm executive director

Cell death mystery yields new suspect for cancer drug development

Public release date: 13-Sep-2012 [ | E-mail | Share ]

Contact: Ellen de Graffenreid edegraff@med.unc.edu 919-962-3405 University of North Carolina Health Care

A mysterious form of cell death, coded in proteins and enzymes, led to a discovery by UNC researchers uncovering a prime suspect for new cancer drug development.

CIB1 is a protein discovered in the lab of Leslie Parise, PhD , professor and chair of the department of biochemistry at the University of North Carolina at Chapel Hill. The small calcium binding protein is found in all kinds of cells.

Cassandra Moran, DO, was a pediatric oncology fellow at UNC prior to accepting a faculty position at Duke University. She is interested in neuroblastoma, a deadly form of childhood brain cancer. While working in the Parise lab at UNC as a resident, she found that decreasing CIB1 in neuroblastoma cells caused cell death.

Cancer is a disease of uncontrolled cell growth, so the ability to cause cancer cell death in the lab is exciting to researchers but the UNC team couldn't figure out how it was happening.

Tina Leisner, PhD, a UNC research associate in biochemistry, picked up where Dr. Moran left off when she returned to her clinical training.

"It was a mystery how loss of CIB1 was causing cell death. We knew that it wasn't the most common mechanism for programmed cell death, called apoptosis, which occurs when enzymes called caspases become activated, leading to the destruction of cellular DNA. These cells were not activating caspases, yet they were dying. It was fascinating, but frustrating at the same time," said Leisner.

What Dr. Leisner and her colleagues found, in the end, is that CIB1 is a master regulator of two pathways that cancer cells use to avoid normal mechanisms for programmed cell death. These two pathways, researchers believe, create "alternate routes" for cell survival and proliferation that may help cancer cells outsmart drug therapy. When one pathway is blocked, the other still sends signals downstream to cause cancer cell survival.

"What we eventually discovered is that CIB1 sits on top of two cell survival pathways, called PI3K/AKT and MEK/ERK. When we knock out CIB1, both pathways grind to a halt. Cells lose AKT signaling, causing another enzyme called GAPDH to accumulate in the cell's nucleus.Cells also lose ERK signaling, which together with GAPDH accumulation in the nucleus cause neuroblastoma cell death. In the language of people who aren't biochemists, knocking out CIB1 cuts off the escape routes for the cell signals that cause uncontrolled growth, making CIB1 a very promising drug target," said Dr. Parise.

The rest is here:
Cell death mystery yields new suspect for cancer drug development

Professor appointed as new director to help courses via technology

Professor appointed as new director to help courses via technology

Center for Teaching Excellence: a program whose goal is to assist faculty with implementing technology-driven course enhancements and advanced features of the electronic course management system.

Source: OU Public Affairs

A new director has been appointed to a program at OU that is designed to help faculty improve courses with new technology.

Teaching strategies expert Mark Morvant, a professor in the department of chemistry and biochemistry, will be appointed Oct. 1 as the executive director of the Center for Teaching Excellence, as long as the OU Board of Regents approves his appointment in its September meeting, according to an OU press release.

Morvant will work with Michele Eodice, associate provost for academic engagement, to embed writing strategies within disciplines across the campus and increase the use of other high-impact instructional techniques, according the press release.

I think the future for the University of Oklahoma is very bright I think theres an excitement among the faculty about improving the educational experience for our students, and Im honored to lead our faculty in improving the students education, Morvant said.

In 2006, Morvant began teaching at OU as a chemistry professor and was named assistant chairman of the chemistry and biochemistry department in 2011, according to the press release.

He will step down from teaching for a few years to build the Center for Teaching Excellence program but plans on eventually returning to limited teaching on a routine basis, Morvant said.

Morvant also will be stepping down from his position as assistant chairman of the chemistry and biochemistry department but will continue to have a faculty appointment in the department, he said.

Read more:
Professor appointed as new director to help courses via technology

Sex Can Cause Genetic Changes In Women

Editor's Choice Main Category: Genetics Also Included In: Biology / Biochemistry Article Date: 12 Sep 2012 - 11:00 PDT

Current ratings for: Sex Can Cause Genetic Changes In Women

5 (1 votes)

A team of researchers from the University of East Anglia set out to determine the response female fruit flies (Drosophila melanogaster) have to mating.

The findings, published in Proceedings of the Royal Society B, indicated that semen consists of a single protein which generates a variety of responses in numerous genes in females, which appears evident at different instances and in different areas of their bodies after mating.

The discovery in the flies, the authors suggest, may be similar to responses in many animals, where semen is inserted into the female's body while having sex.

According to research earlier this year in PLoS Biology, neurodegenerative disorders that occur in both fruit flies and humans are caused by mutations in the same gene, showing that it is plausible that humans may experience the same effect during sex that fruit flies do with the activation of genes.

Scientists have been aware that males pass on seminal fluid proteins to their partner while mating, impacting their feeding, sleep patterns, immunity, egg laying, sexual receptivity, and water balance.

Professor Tracey Chapman, from UEA's school of Biological Sciences and head author, said:

Researchers identified significant changes to genes linked to:

Go here to see the original:
Sex Can Cause Genetic Changes In Women

Novel non-antibiotic agents against MRSA and common strep infections

Public release date: 12-Sep-2012 [ | E-mail | Share ]

Contact: Jessica Studeny jessica.studeny@case.edu 216-368-4692 Case Western Reserve University

Menachem Shoham, PhD, associate professor of biochemistry at Case Western Reserve University School of Medicine, has discovered novel antivirulence drugs that, without killing the bacteria, render Methicillin Resistant Staphylococcus Aureus (MRSA) and Streptococcus pyogenes, commonly referred to as strep, harmless by preventing the production of toxins that cause disease. The promising discovery was presented this week at the Interscience Conference on Antimicrobial Agents and Chemotherapy in San Francisco.

MRSA infections are a growing public health concern, causing 20,000 to 40,000 deaths per year in the United States alone. It is the most prevalent bacterial pathogen in hospital settings and in the community at large, with about one million documented infections per year nationally, costing an estimated $8 billion annually to treat.

The problem has become increasingly severe as the bacteria have developed a resistance to antibiotics. As result, health care providers are running out of options to treat patients suffering from antibiotic-resistant infections, like MRSA and strep, creating a dire need for alternative treatments and approaches.

"Staph bacteria are ubiquitous and normally do not cause infections, however, occasionally these bacteria become harmful due to their secretion of toxins," says Dr. Shoham. "We have discovered potential antivirulence drugs that block the production of toxins, thus rendering the bacteria harmless. Contrary to antibiotics, these new antivirulence drugs do not kill the bacteria. Since the survival of the bacteria is not threatened by this approach, the development of resistance, like that to antibiotics, is not anticipated to be a serious problem."

Dr. Shoham identified a bacterial protein, known as AgrA, as the key molecule responsible for turning on the release of toxins. AgrA, however, needs to be activated to induce toxin production. His goal was to block the activation of AgrA with a drug, thus preventing the cascade of toxin release into the blood that can lead to serious infections throughout the body.

The screening for AgrA inhibitors was initially carried out in a computer by docking libraries of many thousands of "drug-like" compounds and finding out which compounds would fit best into the activation site on AgrA. Subsequently, about 100 of the best scoring compounds were tested in the laboratory for inhibition of the production of a toxin that ruptures red blood cells. Seven of these compounds were found to be active. Testing compounds bearing chemical similarity to the original compounds lead to the discovery of additional and more potent so-called "lead" compounds.

Optimization of the initial "lead" compounds was performed by chemical synthesis of 250 new compounds bearing small but important chemical modifications on one of the initial leads. More than a dozen active compounds have been discovered by this method. The best drug candidate reduces red blood cell rupture by 95 percent without affecting bacterial growth.

Beginning this fall, Dr. Shoham and colleagues will begin testing the drug candidate in animal models.

View post:
Novel non-antibiotic agents against MRSA and common strep infections

BYU breakthrough targets birth defects – BYU biochemistry professor Emily Bates has made recent discoveries that may …

BYU biochemistry professor Emily Bates has made recent discoveries that may revolutionize medicine

BYU research has shed light on the cause and prevention of birth defects as well as cancer.

BYU biochemistry professor Emily Bates and a few of her students recently preformed and published research that may lead to a permanent answer for birth defects and impact how cancer is treated.

Fetal Alcohol Syndrome anda rare condition called Andersen-Tawil Syndrome both cause birth defects like cleft palates, small or missing teeth andmisshapedor connected fingers and toes. Andersen-Tawil Syndrome is caused by genetic changes in a potassium channel, which is also the same channel blocked by consumption of alcohol.

Bates and her students made the revolutionary discovery that potassium channels help cells receive instructions that tell them what they are and where they should be.

Dr. Bates in the research lab

The instructions for cells to divide and move need to be sent during pregnancy while a baby is developing, but those signals should turn off after the baby is born so the cells stay where they are. In cancer cells, the signal has turned back on, allowing cells to metastasize or invade other tissues and allow for growth of new tumors.

Not only are Bates and her students excited to have found some information about the causes of Andersen-Tawil and Fetal Alcohol Syndrome, they are also excited to test a possible therapy to stop the spread of cancer cells throughout the body.

What happens later on in life if someone gets cancer, is that this pathway turns on when its not supposed to turn on anymore, Bates said. The cancer cells start to metastasize, or invade another tissue causing more tumors. What we hope is that blocking this channel will block a signaling pathway that drives metastasis.

In other words, if Bates and her students can eventually find a way to block the channel after it opens back up, cancer cells will not spread throughout the body once the original tumor is removed.

See the rest here:
BYU breakthrough targets birth defects - BYU biochemistry professor Emily Bates has made recent discoveries that may ...

Birth-defect mechanism found by BYU biochemists

Public release date: 11-Sep-2012 [ | E-mail | Share ]

Contact: Joe Hadfield joe_hadfield@byu.edu 801-422-9206 Brigham Young University

The cellular cause of birth defects like cleft palates, missing teeth and problems with fingers and toes has been a tricky puzzle for scientists.

Now Professor Emily Bates and her biochemistry students at Brigham Young University have placed an important piece of the developmental puzzle. They studied an ion channel that regulates the electrical charge of a cell. In a new study published by the journal Development, they show that blocking this channel disrupts the work of a protein that is supposed to carry marching orders to the nucleus.

Without those instructions, cells don't become what they were supposed to become be that part of a palate, a tooth or a finger. Though there are various disorders that lead to birth defects, this newly discovered mechanism may be what some syndromes have in common.

Bates and her graduate student, Giri Dahal, now want to apply the findings toward the prevention of birth defects particularly those caused by fetal alcohol syndrome and fetal alcohol spectrum disorder.

"What we think might be the case is that this is the target for a few similar disorders," Bates said. "The big thing that we have right now is that this ion channel is required for protein signaling, which means that developmental signaling pathways can sense the charge of a cell. And that's exciting for a lot of different reasons."

For example, the new study might also have implications for the battle against cancer. With cancer, the problem is that cells are receiving a bad set of instructions that tells them to multiply and spread. If they can devise a way to block the ion channel, it may stop those cancerous instructions from getting through.

"This protein signaling pathway is the same one that tells cancer cells to metastasize," Bates said. "We're planning to test a therapy to specifically block this channel in just the cells that we want to stop."

Bates, who received her Ph.D. in genetics from Harvard, authored the study with several BYU students. The experience has already helped launch two students into prestigious graduate programs: Brandon Gassaway is at Yale for a Ph.D. in molecular biology and Ben Kwok is at Ohio State University for dental school.

Original post:
Birth-defect mechanism found by BYU biochemists

‘Mad Cow’ blood test now on the horizon

Public release date: 11-Sep-2012 [ | E-mail | Share ]

Contact: Associate Professor Andrew Hill a.hill@unimelb.edu.au 61-425-784-778 University of Melbourne

Using newly available genetic sequencing scientists discovered cells infected with prions (the infectious agent responsible for these diseases) release particles which contain easily recognized 'signature genes'.

Associate Professor Andrew Hill from the Department of Biochemistry and Molecular Biology at the Bio21 Institute said these particles travel in the blood stream, making a diagnostic blood test a possibility.

"This might provide a way to screen people who have spent time in the UK, who currently face restrictions on their ability to donate blood," he said.

"With a simple blood test nurses could deem a prospective donor's blood as healthy, with the potential to significantly boost critical blood stocks."

Mad Cow disease was linked to the deaths of nearly 200 people in Great Britain who consumed meat from infected animals in the late 1980s.

Since 2000, the Australia Red Cross Blood Service has not accepted blood from anybody who lived in the UK for more than six months between 1980 and 1996, or who received a blood transfusion in the UK after 1980.

The research is published in this week's Oxford University Press Nucleic Acids Research journal http://nar.oxfordjournals.org/content/early/2012/09/08/nar.gks832.full.

Lead author Dr Shayne Bellingham said the breakthrough might also help detect other human neurodegenerative diseases, such as Alzheimer's and Parkinson's.

Read more from the original source:
'Mad Cow' blood test now on the horizon

PASSINGS: Robert Morgan Fink, Gene Vollnogle, Dorothy McGuire Williamson

Robert Morgan Fink

Biochemist at UCLA

Robert Morgan Fink, 96, a retired UCLA biochemistry professor whose groundbreaking research with his biochemist wife included developing a new technique in the late 1940s to study the thyroid, died Wednesday of natural causes at his Pacific Palisades home, said Suzanne Coppenrath, one of his two daughters.

He was a pioneer who "is remembered as a very good scientist who did important work," said Elizabeth Neufeld, former chairwoman of the department of biological chemistry at the David Geffen School of Medicine at UCLA.

At the University of Rochester, Fink met his future wife, Kathryn, a fellow graduate student. After marrying in 1941, they worked together at Rochester on the Manhattan Project, which would produce the atom bomb.

The head of the project at Rochester was Dr. Stafford Warren, who recruited the Finks to join the UCLA faculty after he was named the first dean of its school of medicine. When the couple came to UCLA in 1947, space for experiments was limited and at first they conducted research at hospitals in the San Fernando Valley and Long Beach.

The Finks were perhaps best known for a 1948 breakthrough in thyroid biochemistry called the "paper chromatography technique." They used radioactive "tracer" chemicals on small samples of the thyroid and other body tissues, which caused them to essentially photograph themselves and expose new and previously inconceivable detail.

The technique worked so well that the Finks were able to isolate and identify a dozen new biological compounds. The approach was later adapted to determine if chemotherapy was helping cancer patients.

In 1978, Robert Fink retired from UCLA as a biochemistry professor. His wife was assistant dean for student affairs at UCLA's medical school when she died at 72 in 1989.

Born Sept. 22, 1915, in Greenville, Ill., he was one of six children of a glove salesman who eventually owned the factory.

Go here to see the original:
PASSINGS: Robert Morgan Fink, Gene Vollnogle, Dorothy McGuire Williamson