New Delhi The Indira Gandhi National Open University (IGNOU) has extended till August 3 the last date of admission for its PhD and MPhil programmes.

IGNOU has invited applications for MPhil in chemistry and geography, PhD in biochemistry, chemistry, French, gender and development studies, geography, geology, journalism and mass communication, fine arts, physics, theatre arts, statistics and womens studies.

IGNOUs research unit director K Barik has said that the last date for PhD and MPhil programmes has been extended till 3 August.

The entrance test for various programmes will be held on August 20 in selected examination centres across the country.

The University, which began academic programmes in 1987, today enrols over three million students in India and other countries through 21 schools of studies and a network of 67 regional centres, around 2,667 learner support centres and 29 overseas partner institutions.

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IGNOU's PhD, MPhil admission date extended to Aug 3 - Hindustan Times

A ribbon diagram of the three-part efflux pump of the Campylobacter jejuni bacterium. Credit: Edward Yu/Iowa State University

Two new discoveries from Edward Yu's Iowa State University laboratory are adding to the scientific understanding of how bacteria resist antibiotics.

Yu and his research group have just described two structures and mechanisms - efflux pumps and reinforced cell walls - that certain disease-causing bacteria use to keep antibiotics away. That understanding could one day lead to new treatments that disable the structures and restore the effectiveness of drugs.

"We study a lot of efflux pumps to understand antibiotic resistance," said Yu, an Iowa State professor with appointments in physics and astronomy; chemistry; biochemistry, biophysics and molecular biology; and the U.S. Department of Energy's Ames Laboratory. "Cell wall remodeling is also a major mechanism to work against antibacterial drugs.

"The structure and mechanism depend on the bacteria you're talking about - and the bacteria will find a way."

Two journals have just published the latest findings by Yu's research group:

Previous studies reported the three molecules of the pump worked in a synchronized rotation - one molecule accessing, one molecule binding and one molecule extruding - to pump antibiotics from the cell. Yu's research group found that each part of the pump worked independently of the others, essentially creating three pumps in one structure.

"The three independent pumps make it a more powerful multidrug efflux pump," Yu said.

The paper focuses on how these bacteria transport hopanoid lipid compounds to their outer cell membranes. The compounds contribute to membrane stability and stiffness.

"Overall our data suggest a novel mechanism for hopanoid transport involved in cell wall remodeling, which is critical for mediating multidrug resistance in Burkholderia," the authors wrote in a project summary.

Grants from the National Institutes of Health supported both studies. Grants from the U.S. Department of Energy also supported ultra-bright, high-energy X-ray experiments at the Advanced Photon Source at Argonne National Laboratory in Illinois.

Yu and his research group have a long history of successfully using X-ray crystallography to describe and understand the structure of pumps, transporters and regulators in bacteria. A gallery on his research group's website shows ribbon diagrams of 21 different structures.

Because of Yu's significant contribution to the understanding of antimicrobial resistance in bacteria, the American Academy of Microbiology elected him to be an academy fellow earlier this year.

With that comprehensive understanding of the structures and mechanisms behind bacterial resistance to antibiotics, Yu said his research group is beginning to look at how the pumps and transporters can be turned off.

"We're trying to find an inhibitor compound," Yu said. "We're thinking about doing a little more translational science. We have a lot of rich information about the structure and function of these pumps. Why not use it?"

Explore further: Scientists describe protein pumps that allow bacteria to resist drugs

More information: Chih-Chia Su et al, Structures and transport dynamics of a Campylobacter jejuni multidrug efflux pump, Nature Communications (2017). DOI: 10.1038/s41467-017-00217-z

Nitin Kumar et al. Crystal structures of theBurkholderia multivoranshopanoid transporter HpnN, Proceedings of the National Academy of Sciences (2017). DOI: 10.1073/pnas.1619660114

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Researchers describe structures, mechanisms that enable bacteria to resist antibiotics - Phys.Org

Decoding aging is one complicated process that scientists across globe are busy working on.

While a revolutionary breakthrough is still awaited, a group of scientists from Allahabad have developed unique model of rat which can go a long way in helping them find a formula to control the process.

Perhaps taking a cue from Bollywood blockbuster Paa, the scientists have developed a model of rat which displays a higher rate of aging.

The accelerated aging model of rat provides a great tool for scientists to study aging and also to test anti-aging drugs, claims prof SI Rizvi from the Biochemistry department of Allahabad University (AU).

Rizvi is leading the research team.

The teams findings and achievement have been published in the recent issue of the prestigious research journal Biochemical and Biophysical Research Communications published from US.

Explaining his new research, prof Rizvi said that his team created a rat model which mimics the human condition of Progeria, a disease in which the patient starts to show a faster rate of aging.

Progeria syndrome was highlighted in the acclaimed Hindi movie Paa wherein the character was portrayed effectively by Amitabh Bachchan.

Progeria is a rare genetic condition that causes a childs body to age fast. Most kids with progeria do not live past the age of 13. The disease affects both sexes and all races equally. It affects about 1 in every 4 million births worldwide. Medical experts believe that India has around 8-10 reported cases of progeria and potentially 66 unreported cases.

To study aging, scientists rely on animal models such as C elegans (an earthworm), fruit flies, and mice. The consideration for choosing an animal is primarily based on its lifespan. Shorter lifespan provides an opportunity to study age-dependent changes in a shorter time frame.

To create the Progeria model of rat, the Allahabad University scientists subjected normal rats to chronic treatment of 30 days with dihydrotachysterol, a chemical similar to vitamin D. A look into relevant scientific literature reveals that very few studies have been conducted on such a model of rat.

Normal experimental rats have a lifespan of two years, which is too large a time for conducting experiments. The rat model mimicking Progeria provides a very good model to study aging process in a short span of time, added prof Rizvi.

The young progeria-mimicking rats display a certain level of oxidative stress (an established hallmark of aging) equivalent to old age rats.

The research group will now test Metformin, a common anti-diabetic drug, as an experimental anti-aging drug on increased aging model rats. Initial results using Metformin as an anti aging drug have been very exciting, added prof Rizvi.

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Allahabad University scientists create 'accelerated ageing model' in ... - Hindustan Times

Marek Michalak, a professor in the University of Alberta's Department of Biochemistry and graduate student Wen-An Wang were part of the team that discovered a direct link between calcium and cholesterol. Credit: Melissa Fabrizio

It's well known that calcium is essential for strong bones and teeth, but new research shows it also plays a key role in moderating another important aspect of healthcholesterol.

Scientists at the University of Alberta and McGill University have discovered a direct link between calcium and cholesterol, a discovery that could pave the way for new ways of treating high blood cholesterol.

The researchers began the work after having their curiosity piqued while studying the role of a calcium-binding protein. They noticed an extreme rise of blood cholesterol concentration in mice when the protein was not present. To follow up on this observation, Marek Michalak with graduate student Wen-An Wang (University of Alberta) and Luis Agellon (McGill University) teamed up with geneticist Joohong Ahnn (Hanyang University, Korea) and discovered that the physiological link between calcium and cholesterol is also preserved in worms.

"There is a mechanism inside the cell that senses when there is not enough cholesterol present and turns on the machinery to make more," said Michalak, a distinguished university professor in the University of Alberta's Department of Biochemistry. "What we found is that a lack of calcium can hide cholesterol from this machinery. If you lose calcium, your synthetic machinery thinks there's no cholesterol and it starts making more even if there is already enough."

High blood cholesterol is a known risk factor for developing heart disease. "Factors that affect blood cholesterol concentration have been studied for a long time," said Agellon, a professor at McGill's School of Human Nutrition. "The general belief was that cholesterol controlled its own synthesis inside of cells, and then we discovered in our labs that calcium can control that function too. Finding this link potentially opens a door to developing new ways of controlling cholesterol metabolism."

The researchers consider their finding a significant step toward developing different approaches to patient care in the future, but there is more work to be done. They are now looking to discover the common factor that allows calcium and cholesterol to communicate with each other in the cell and have received a four-year grant worth $456,000 from the Canadian Institutes of Health Research to continue their work.

Explore further: What you need to know about cholesterol

More information: Wen-An Wang et al, Loss of Calreticulin Uncovers a Critical Role for Calcium in Regulating Cellular Lipid Homeostasis, Scientific Reports (2017). DOI: 10.1038/s41598-017-05734-x

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Scientists uncover a hidden calcium cholesterol connection - Phys.org - Phys.Org

Titan, partially obscured by Saturns rings. Image: NASA/JPL-Caltech/Space Science Institute

Saturns moon Titan is a world of contrast; both eerily familiar and strikingly alien. Its calm seas and enormous sand dunes might remind you of Earth, until you learn that whats flowing across Titans surface is not water, but liquid hydrocarbons. Titans nitrogen-rich atmosphere seems to have some of the ingredients for biology, but any life forms evolved to thrive at temperatures of -290 degrees Fahrenheit would be practically unrecognizable.

A new scientific paper supports the idea that life might exist on Titan, but that it would be nothing like life as we know it. After studying spectroscopic data collected by the Atacama Large Millimeter/sub millimeter Array (ALMA) in northern Chile, researchers are now reporting that Titans atmosphere is rife with vinyl cyanide, a molecule that could, in theory, form cell-like membranes under the moons unique environmental conditions.

In fact, based on the levels of vinyl cyanide present in Titans atmosphere, its seas couldin theory, were not saying there are aliensbe bubbling with tiny cell membranes, with concentrations similar to those of bacteria in Earths oceans.

The membranes that enclose the cells of all living things here on Earth are made of phospholipids, molecules with long, non-polar (water-repelling) tails and polar (water-loving) heads. If you remember high school biology, youll know that phospholipids form a bi-layer, with the water-loving parts on the outside, and the water-repelling bits on the inside. This structure allows membranes to bubble off tiny pockets of water from their surroundings, creating cells that house genetic material and support biochemical reactions.

Thats all well and good for organisms evolved to thrive in the temperate, liquid water seas here on Earth, but the membranes our biology uses simply wouldnt work in the cryogenic methane seas of Titan. (Theyd be far too rigid, and water-loving/water-repelling bits would have to be reversed.) So, what could cells on Titan look like? Two years back, researchers at Cornell University used chemical models to attempt to answer that very question. Through those models, they produced a functional cell membrane that remained stable and flexible at incredibly low temperatures, using none other than C2H3CN, or vinyl cyanide.

They called their hypothetical alien cell an azotosome.

What makes vinyl cyanide potentially useful molecule for this is that its amphiphilicit has a polar and a non polar end, just like our membranes phospholipids, Maureen Palmer, a recent graduate of St. Olaf College and lead author on the new study,explained. It would be sort of the same but sort of the opposite of how cell membrane lipids work on Earth, with the polar bits on the inside, and the non-polar bits on the outside.

It was a fascinating hypothesis, but there was one problemnobody had ever confirmed that vinyl cyanide is actually present on Titan. (NASAs Cassini spacecraft found tentative evidence for the molecule several years back.) Palmerand her colleagues decided to fill in this gap, by examining calibration data ALMA collects at Titan before turning its telescopes to stare at other targets. Sure enough, they found compelling evidence that large amounts of vinyl cyanide are present in Titans atmospheremainly, at altitudes greater than 200 kilometers. The research was published today in Scientific Reports.

When I sent the paper to Jonathan Lunine, Cornell astronomer and co-author on the 2015 study positing the existence of azotosomes, he said it was quite gratifying to see that acrylonitrile, or vinyl cyanide, does indeed seem to be present in Titans atmosphere.

Of course, life as we know it would be more likely to emerge in the vast seas on Titans surface than high up in the sky. But as Palmer and her colleagues point out, rainfall is constantly transporting organic compounds to Titans surfaceand those could include vinyl cyanide. It should be reaching the surface, she said. Titan has lots of rain.

In fact, in Ligeia Mare, a methane sea larger than Michigans Lake Superior located near Titans north pole, Palmer and her colleagues estimate there could be as many as 30 million azotosomes per cubic centimeter of sea water. For comparison, costal ocean waters on Earth have about a million bacteria per cubic centimeter, according to one papers estimate.

This is a crucial point and lab experiments ought to be done, Lunine added. Palmer agreed.

Im hoping someone will do a study of trying to form the membranes in the lab, seeing if theyre actually able to form, she said. Her co-authors are currently trying to better constrain the abundance and distribution of vinyl cyanide in Titans atmospherethis first paper was just a rough look. Theyre also searching for evidence of other biologically-relevant molecules on Titan. Also this week, another team of scientists reported the detection of carbon chain anionspotential building blocks of complex biomoleculesin Titans upper atmosphere, using data from Cassini.

Ultimately, resolving the question of whether or not Titan is home to some seriously weird life forms will require a future mission that can land on its surfacemaybe a cryogenic methane-proof submarine. Palmer is definitely rooting for a lander.

I love Titan, Palmer said. Its super interesting as an astrobiology target, because all forms of life we know of on Earth have water as the solvent, but it has liquid methane. It would be a totally different form of biochemistry, if there was life on Titan. I find that possibility fascinating.

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Molecules That Could Form 'Cell-Like' Membranes Spotted on Saturn's Largest Moon - Gizmodo

A champion of modern molecular genetics, Model asked questions that changed the way research was conducted. (Photo by Ingbert Grttner, 1988)

Peter Model, an emeritus faculty member who spent the major part of his career at The Rockefeller University, died on June 9 at the age of 84, after a brief period of declining health. Model used genetics, biochemistry, and molecular biology to study the f1 phage, a type of virus that infects Escherichia coli bacteria. His work provided valuable details about the way genes express themselves and control one another.

Peter brought an incisive, inquisitive mind to his research, and was often responsible for the astute question that would push an investigation in the right direction, noted Rockefeller President Richard P. Lifton in a message to university faculty and staff. He enjoyed the camaraderie of his fellow scientists, served as an informal mentor to many junior faculty members who sought his advice, and was an active member of the Rockefeller community until very recently.

Born in Frankfurt in 1933 during the rise of the Nazis, Model and his parents escaped in 1942 to settle in New York. As a young man, he studied economics at Cornell University and Stanford University, served in the United States Army as a first lieutenant, and worked in his fathers investment banking business for a period before earning a Ph.D. in biochemistry from Columbia University.

Peter was a remarkable person who straddled many worlds, says Jeffrey V. Ravetch, Theresa and Eugene M. Lang Professor and head of the Leonard WagnerLaboratory of Molecular Genetics and Immunology at Rockefeller, who was a student in Models lab in the mid-1970s. Perhaps because of his background in economics and finance, he had a different way of looking at things, and he became a great champion of using new approaches in the lab. He was viciously smart, and he always valued substance over style.

When many other people began working with mammalian systems, Peter stuck to his focus on bacterial genetics and remained true to the essence of microbial systems, Ravetch adds. He saw that they would continue to yield valuable discoveries.

Model arrived at Rockefeller in 1967, joining the laboratory of the late Norton Zinder as a postdoctoral fellow. Named assistant professor in 1969 and associate professor in 1975, he was promoted to full professor in 1987. He and Zinder worked closely together in the laboratory, and Model became co-head of the lab in 1987. From 1992 to 1995, he also served as associate dean of curriculum under deans Bruce McEwen and later Zinder.

Bacterial viruses, or phages, are among the simplest of biological entities and contain only a handful of genes. Models work with them opened a number of new lines of research. He championed the use of several modern molecular genetic techniques, and used these methods to examine, among other things, how phage proteins translocate across bacterial membranes. He developed phage display, which became a widely used method for identifying interactions between proteins. Using this and other techniques, he explored key biochemical processes in the lifecycles of phages.

Models strong commitment to the education and training of younger scientists led him to serve as the primary advisor for a number of graduate students and postdocs during his tenure at Rockefeller.

Peter had a way of asking questions that could change the direction of research, says his wife, Rockefeller associate professor Marjorie Russel, with whom he collaborated. He was famous for incorporating his knowledge from diverse areas and putting everything together in ways that no one else had ever thought of before. Often, after talking to Peter, his students and colleagues would go back to their lab benches with completely new ideas about what to do and where to go with their research.

In addition to his wife, Model is survived by his children, Paul and Sascha; his brother, Allen; and four grandchildren, as well as many other relatives and friends.

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Geneticist and Rockefeller emeritus Peter Model dies at 84 - The Rockefeller University Newswire

COLLEGEVILLE >> U.S. Rep. Ryan Costello, R-6th Dist., visited Ursinus College on July 6 to announce a National Science Foundation grant.

The grant was in the amount of $28,531 for the project, Collaborative Research, which is researching using protein function prediction to promote hypothesis-driven thinking in undergraduate biochemistry education.

Costello, a member of the STEM Caucus, had the opportunity to meet with Rebecca Roberts, an associate professor of biology, and biochemistry and molecular biology at Ursinus College, as well as several students to hear about their research projects.

Im pleased to see students in our community will benefit from a grant that will enable first-hand experiences to encourage them to think like a scientist and, in turn, explore opportunities in STEM education. This grant will also help faculty understand how students learn from these techniques, Costello said in a prepared release.

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I am aiming to provide even greater opportunities for Ursinus students to experience authentic research by bringing research into their courses. As part of a collaboration with faculty from across the country, I have helped develop a project that challenges students to discover functions for proteins of known structure but with currently unknown function. This grant from the National Science Foundation will allow us to continue to engage our students in this project and to evaluate the impact of the experience on their growth as scientists, said Roberts.

Costello recently signed a bipartisan letter to the House Appropriations Committee requesting robust, continued funding for the NSF in the upcoming 2018 Fiscal Year, and has introduced and supported several pieces of legislation to support students who choose STEM fields.

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Ursinus College gets biochemistry grant from National Science foundation - The Times Herald

Vermont Business Magazine The Northern New England population will be the beneficiary of a new partnership between academic medical centers and primary care practices in rural communities, which will focus on health problems endemic to the region, including cancer, cardiovascular disease, substance abuse, as well as the unique challenges of effective rural health care delivery. A five-year, $20 million National Institutes of Health (NIH) Clinical and Translational Research (CTR) Network grant will fund a joint program between the University of Vermont (UVM) and Maine Medical Center in Portland, Maine to develop and sustain a clinical and translational research infrastructure improving rural and community health for residents of Vermont, New Hampshire and Maine. The grant, awarded through the federally-funded IDeA program, enhances research efforts in states where NIH funding levels have traditionally been lower and rural and medically-underserved communities are a priority.

The program will be collaboratively led by principal investigators Gary Stein, Ph.D., UVM Cancer Center director and Department of Biochemistry chair, and Clifford Rosen, M.D., senior scientist at Maine Medical Center Research Institute. UVM Larner College of Medicine Senior Associate Dean for Research Gordon Jensen, M.D., Ph.D., and Thomas Gridley, Ph.D., interim director of the Center for Molecular Medicine at Maine Medical Center Research Institute, will serve as the grants program coordinators.

According to Jensen, Vermont, New Hampshire and Maine have a similar geographic distribution of patients. This will allow participating primary care physicians to work in partnership with academic medical centers to carry out the programs research initiatives and to meet the needs and challenges throughout the northern New England region.

As a cancer center director, Stein emphasizes the capabilities of the networks six program components to address the underlying causes of the regions greatest health threats from multiple perspectives using a rich variety of expertise and collaborative resources and to make related diseases preventable and treatable.

This grant will allow us to investigate the most effective ways to address shared health care issues, said Stein. The program will derive great benefit from maximally engaging the breadth of expertise we have at the University in concert with our primary care partners.

UVM faculty will co-lead five of the six program areas with faculty from Maine Medical Center. Jan Carney, M.D., M.P.H., associate dean for public health, will co-lead Rural Health Research and Delivery; Frances Carr, Ph.D., professor of pharmacology, will co-lead Translational Research Technologies; Bernard Cole, Ph.D., professor of mathematics and statistics, will co-lead Clinical Research Design, Epidemiology; Jane Lian, Ph.D., professor of biochemistry, will co-lead the Pilot Projects Program; and Kim Luebbers, M.S.H.S., R.N., assistant dean for clinical research, will co-lead Professional Development, Clinical Research Design, Epidemiology. The Tracking and Evaluation program will be led by faculty from the University of Southern Maine.

This $20 million grant reinforces confidence in the tremendous resource that is provided by the Universitynot just in education, but in promoting and protecting the overall health and well-being of our citizens, said Vermont Health Commissioner Mark Levine, MD.Collaborations with the Department of Health will leverage these capabilities to make a difference for Vermonters wherever they live.

Source: UVM 7.12.2017

VBM vermontbiz.com

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NIH awards $20 million to UVM and Maine Medical to address rural health challenges - Vermont Biz

(From left are) Drs. B.R. Achyut; Thaiz F. Borin, postdoctoral fellow and a corresponding author; and Ali S. Arbab. Credit: Phil Jones

It's a metabolite found in essentially all our cells that, like so many things, cancer overexpresses. Now scientists have shown that when they inhibit 20-HETE, it reduces both the size of a breast cancer tumor and its ability to spread to the lungs.

"The drug is reducing the ability of cancer cells to create a distant microenvironment where they can thrive," said Dr. Ali S. Arbab, leader of the Tumor Angiogenesis Initiative at the Georgia Cancer Center and a professor in the Department of Biochemistry and Molecular Biology at the Medical College of Georgia at Augusta University.

Arbab notes that cancer cells are constantly doing test runs, sending cells out into the bloodstream to see if they will take hold. About 30 percent of patients with breast cancer experience spread, or metastasis, of the disease. The most common sites are the lymph nodes, liver, bones and brain, as well as the lungs.

For the preclinical studies by postdoctoral fellow, Dr. Thaiz F. Borin, published in the journal PLOS ONE, the scientists used the drug HET0016, a 20-HETE inhibitor developed to learn more about the metabolite's many functions.

While not ready to say that the drug has potential use in humans, Arbab says the work points toward a new and logical target for reducing tumor spread. He notes that there are already drugs out there, including some over-the-counter anti-inflammatory drugs, which may also inhibit this overexpressed and now destructive pathway.

20-HETE - 20-Hydroxyeicosatetraenoic acid - is a metabolite of arachidonic acid, a fatty acid we make and constantly use for a wide variety of functions like helping make lipids for our cell membranes. 20-HETE also has a wide range of normal functions, including helping regulate blood pressure and blood flow. It's also a known mediator of inflammation, which under healthy conditions can help us fight infection and protect us from cancer and other invaders.

"There is normal function and there is tumor-associated function," says Dr. B.R. Achyut, cancer biologist, assistant professor in the MCG Department of Biochemistry and Molecular Biology and a study coauthor. "Tumors highjack our system and use that molecule against us."

In fact, Arbab's research team has shown that the high production of 20-HETE that occurs in cancer becomes an unwitting provider of almost everything cancer needs to prepare a place to comfortably spread.

Scientists call it the "seed and soil" hypothesis. To spread, cancer cells must detach from the primary site, in this case breast tissue, get aggressive enough to survive travel, gather supporting tissue and blood vessels where they land, take seed and eventually colonize the distant site, in this case, the lungs.

Arbab and his team have shown 20-HETE appears to help prepare this distant site by activating things like protein kinases that can change the function of proteins, their location and what cells they associate with, as well as growth factors that can make cells grow in size, proliferate and differentiate. It can even help make blood vessels, which a tumor will need once it reaches a certain size. 20-HETE also activates signaling kinases that enable cell division. It encourages inflammation-promoting factors like tumor necrosis factor alpha and several of the interleukins, another class of proteins that help regulate the immune response. In this scenario, they are turning up inflammation, which is a hallmark of cancer and other diseases.

"We are going after that tumor microenvironment," says Arbab.

For their studies, they put human breast cancer cells and mouse mammary tumor cells in the mammary fat pad of mice, waited for the cancer to take hold and begin to spread, then intravenously gave mice HET0016 five days per week for three weeks.

They found HET0016 reduced the migration and invasion of tumor cells: 48 hours after the drug was given, cancer cells were less able to move about in small test tubes. The drug also reduced levels of metalloproteinases in the lungs, enzymes that can destroy existing protein structures, so that, in this case, cancer cells can penetrate the area and new blood vessels can grow. It also reduced levels of other key inhabitants of a tumor microenvironment like growth factors as well as myeloid-derived suppressor cells that can help shield cancer from the immune system. "It gets rid of one of the natural protections tumors use, and tumor growth in the lung goes down," Arbab notes.

He, Achyut and their colleague Dr. Meenu Jain, assistant research scientist, reported earlier this year in the journal Scientific Reports that the drug also reduced tumor growth and prolonged survival in an animal model of the highly lethal, rapidly growing and vascular brain tumor, glioblastoma. That finding and related work got the scientists wondering if the research drug - or something similar - could one day help control the typically deadly spread of cancer.

Now they are looking at exosomes, traveling packages all cells send out as a way to communicate and swap substances. In the case of cancer cells, exosomes appear to be packed with items needed to build the supportive environment for their new distant location in the lungs or elsewhere. Once exosomes establish a niche, they send back a signal to the primary site for cancer cells to join them. The scientists want to further pursue the ability of HET0016 to block these cancer-derived packages.

20-HETE's co-opting by cancer has it emerging as a focal point for cancer treatment, says Arbab who has published more than half of the 20-HETE-related studies on the rapidly emerging topic.

Explore further: Cells that make blood vessels can also make tumors and enable their spread

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Spread of breast cancer reduced by targeting acid metabolite - Medical Xpress

Columbia Johnson County students are named to the College of Agriculture, Food and Natural Resources deans list at the University of Missouri.

Harrison Bron, food science and nutrition, and Jared Yates, biochemistry, both of Knob Noster; and Emma Downing, agricultural economics, and Matthew Lichte, biochemistry, both of Warrensburg, made the list.

Being named to the deans list is an exceptional academic accomplishment,"Bryan Garton, associate dean and director of academic programs, said in a statement. "We are very proud of each student, not only for their academic excellence, but also for the hard work and dedication to their academics and career preparation this past semester.

Students must maintain a term GPA of 3.3, a cumulative GPA of 3.0 and be enrolled in a minimum of 12 credit hours to be named on the CAFNR deans list.

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Johnson County students make dean's list - The Daily Star-Journal