OREGON STATE UNIVERSITY

college of science

Licensing agreement reached on brilliant new blue pigment discovered by happy accident

CORVALLIS, Ore. – A brilliant new blue pigment – discovered serendipitously by Oregon State University chemists in 2009 – is now reaching the marketplace, where it will be used in a wide range of coatings and plastics.

The commercial development has solved a quest that began thousands of years ago, and captured the imagination of ancient Egyptians, the Han dynasty in China, Mayan cultures and others – to develop a near-perfect blue pigment.

It happened accidently.

OSU chemist Mas Subramanian and his team were experimenting with new materials that could be used in electronics applications and they mixed manganese oxide – which is black in color – with other chemicals and heated them in a furnace to nearly 2,000 degrees Fahrenheit. One of their samples turned out to be a vivid blue. Oregon State graduate student Andrew Smith initially made these samples to study their electrical properties.

“It was serendipity, actually; a happy, accidental discovery,” Subramanian said.

The new pigment is formed by a unique crystal structure that allows the manganese ions to absorb red and green wavelengths of light, while only reflecting blue. The vibrant blue is so durable, and its compounds are so stable – even in oil and water – that the color does not fade.

These characteristics make the new pigment versatile for a variety of commercial products. Used in paints, for example, they can help keep buildings cool by reflecting infrared light. Better yet, Subramanian said, none of the pigment’s ingredients are toxic.

OSU has reached an exclusive licensing agreement for the pigment, which is known as “YInMn” blue, with The Shepherd Color Company. It will be used in a wide range of coatings and plastics.

“This new blue pigment is a sign that there are new pigments to be discovered in the inorganic pigments family,” said Geoffrey T. Peake, research and development manager for The Shepherd Color Company. Commercial quantities of the pigment will be available later this year, he added.

The lack of toxic materials is critical, Subramanian pointed out, and a hallmark of the new pigment.

“The basic crystal structure we’re using for these pigments was known before, but no one had ever considered using it for any commercial purpose, including pigments,” Subramanian said.  “Ever since the early Egyptians developed some of the first blue pigments, the pigment industry has been struggling to address problems with safety, toxicity and durability.”

Another commercial use of the product – in addition to coatings and plastics, may be in roofing materials. The new pigment is a “cool blue” compound that has infrared reflectivity of about 40 percent – much high than other blue pigments – and could be used in the blue roofing movement.

“The more we discover about the pigment, the more interesting it gets,” said, Subramanian, who is the Milton Harris Professor of Materials Science in the OSU College of Science.  “We already knew it had advantages of being more durable, safe and fairly easy to produce. Now it also appears to be a new candidate for energy efficiency.”

In addition to testing the blue pigment for other applications, Subramanian is attempting to discover new pigments by creating intentional laboratory “accidents.” His original work was funded by the National Science Foundation.

“Who knows what we may find?,” he said.

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Mas Subramanian, 541-737-8235, mas.subramanian@oregonstate.edu

New zebrafish model should speed research on parasite that causes toxoplasmosis

 

The study this story is based on is available online: http://bit.ly/1e2jPlB

CORVALLIS, Ore. – Researchers at Oregon State University have found a method to speed the search for new therapies to treat toxoplasmosis – by successfully infecting zebrafish with Toxoplasma gondii.

The findings were just published in the Journal of Fish Diseases, in work supported by the Tartar Foundation and the National Institutes of Health.

T. gondii, a protozoan parasite, can infect a wide range of hosts, and is one of the most prevalent parasites in the world. It has been estimated to infect about one-third of the human race. Treatment can be difficult because parasites often have biologic similarities to the hosts they infect.

Zebrafish have been found in recent years to be an excellent model for biomedical research because they reproduce rapidly, bear many similarities to human genetics and biological systems, and can be used in “high throughput” technologies to literally test hundreds of compounds in a fairly short period of time.

“This advance may provide a very efficient tool for the discovery of new therapies for this parasitic infection,” said Justin Sanders, an OSU postdoctoral fellow and lead author on the study. “With it we should be able to more easily screen a large library of compounds, at much less expense, and look at things that are unknown or have never been considered as a possible treatment.”

Although it infects many animals, T. gondii infection has never been observed prior to this in fish. But the OSU researchers found that by raising the temperature of the water in which zebrafish lived to a warmer-than-normal 98.6 degrees, or the temperature of a human body, they could become infected with the parasite but also survive.

T. gondii affects a wide range of mammals and birds, and cats are actually one of the most routine hosts,” said Michael Kent, a professor of microbiology in the OSU College of Science. “It can cause congenital defects, which is one reason that pregnant women are told not to clean the catbox. Many people become infected for life. These chronic infections can cause serious eye disease and can be fatal to people with weakened immune systems.

“New therapies would clearly be of value, and now we have a better way to find them,” he said.

This work was done in collaboration with researchers from the University of Chicago, Albert Einstein College of Medicine, and the U.S. Department of Agriculture.

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Michael Kent, 541-737-8652

Disrupted biological clock linked to Alzheimer’s disease

CORVALLIS, Ore. – New research has identified some of the processes by which molecules associated with neurological diseases can disrupt the biological clock, interfere with sleep and activity patterns, and set the stage for a spiral of health concerns that can include a decreased lifespan and Alzheimer’s disease.

The research was published in Neurobiology of Disease by scientists from Oregon State University and the Oregon Health & Science University, in work supported by the National Institutes of Health.

Previous studies have shown that disruption of the biological clock – the natural pattern of day-night activity that’s genetically controlled in many animals – can cause neurodegeneration, loss of motor function and early death.

The newest results help outline the molecular mechanisms involved, and show how proteins associated with neurological disease can diminish the biological clock function and ultimately lead to very serious health problems, including severe cognitive deterioration. It also confirms that these risks increase significantly with age.

"The molecular basis underlying biological clock deficits in Alzheimer's disease has been difficult to tease out," said Matthew Blake, an OSU faculty research assistant and author of the study. "Only recently have we been able to utilize our model system to accurately dissect this mechanism."

This research was done with fruit flies, which have many genes and biological processes that are similar or identical to those of humans, retained through millions of years of evolution. Circadian clocks are so essential to health that they are found throughout the nervous system and peripheral organs.

Proper function of circadian rhythms has been shown to affect everything from sleep to stress reaction, feeding patterns, DNA repair, fertility and even the effectiveness of medications.

“Alzheimer’s disease has always been of interest in this research, because sleep disruption is one of its earliest symptoms, and almost everyone with Alzheimer’s has some sleep problems,” said Jadwiga Giebultowicz, corresponding author of this study, a professor in the Department of Integrative Biology in the OSU College of Science, and expert on the biological and genetic underpinnings of the biological clock.

“This research adds more support to the hypothesis that neurological damage is a circular process that, in turn, causes more disruption of the biological clock,” Giebultowicz said. “We’ve identified a new player in this process, a fragment of the amyloid precursor protein called AICD, that is able to enter the nucleus of cells and interfere with central clock function.”

One known cause of Alzheimer’s disease is cleavage of an amyloid precursor protein, which creates a peptide that’s toxic to neurons. An enzyme involved is elevated in Alzheimer’s patients. This study took that process further and showed that increased production of the enzyme, which in flies is called dBACE, reduced the expression of a core clock protein.

The results suggest that dBACE acts via dAICD to cause the disruption of the biological clock and loss of daily sleep and activity cycles. This disruptive process was much more severe in older flies.

“A general message from this is that normal day-night, sleep and activity cycles are important,” Giebultowicz said.

“There’s evidence that proper sleep allows neuronal repair activity and the maintenance of neuronal health,” she said. “Since neuronal damage is a destructive process that can build on itself once it begins, it’s important that sleep issues should be taken seriously by people and their doctors, especially as they age.”

Molecular clock oscillations decline with age, Giebultowicz said, and finding ways to help maintain or restore them might form the basis for a possible therapy to reduce or prevent the associated health problems.

Collaborators on this research included Eileen Chow in the Department of Integrative Biology at OSU, and Doris Kretzschmar at the Oregon Institute of Occupational Health Sciences, an international expert in the use of fruit flies as a model for neurodegenerative diseases.

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Jadwiga Giebultowicz, 541-737-5530

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Drosophila melanogaster
Fruit fly

A mile deep, ocean fish facing health impacts from human pollution

CORVALLIS, Ore. – Deep-water marine fish living on the continental slopes at depths from 2,000 feet to one mile have liver pathologies, tumors and other health problems that may be linked to human-caused  pollution, one of the first studies of its type has found.

The research, conducted in the Bay of Biscay west of France, also discovered the first case of a deep water fish species with an “intersex” condition, a blend of male and female sex organs. The sampling was done in an area with no apparent point-source pollution, and appears to reflect general ocean conditions.

The findings have been published in Marine Environmental Research, by scientists from Oregon State University; the Centre for Environment, Fisheries and Aquaculture Science in the United Kingdom; and other agencies. It was supported by the European Union.

The research is of particular interest, OSU researchers said, when contrasted to other studies done several years ago in national parks of the American West, which also found significant pollution and fish health impacts, including male fish that had been “feminized” and developed eggs.

“In areas ranging from pristine, high mountain lakes of the United States to ocean waters off the coasts of France and Spain, we’ve now found evidence of possible human-caused pollution that’s bad enough to have pathological impacts on fish,” said Michael Kent, a professor of microbiology in the OSU College of Science, co-author on both these research projects and an international expert on fish disease.

“Deep in the ocean one might have thought that the level of contamination and its biological impact would be less,” Kent said. “That may not be the case. The pathological changes we’re seeing are clearly the type associated with exposure to toxins and carcinogens.”

However, linking these changes in the deep water fish to pollution is preliminary at this time, the researchers said, because these same changes may also be caused by naturally-occurring compounds. Follow up chemical analyses would provide more conclusive links with the pathological changes and man’s activity, they said.

Few, if any health surveys of this type have been done on the fish living on the continental slopes, the researchers said. Most past studies have looked only at their parasite fauna, not more internal biological problems such as liver damage. The issues are important, however, since there’s growing interest in these areas as a fisheries resource, as other fisheries on the shallower continental shelf become depleted.

As the sea deepens along these continental slopes, it’s been known that it can act as a sink for heavy metal contaminants such as mercury, cadmium and lead, and organic contaminants such as PCBs and pesticides. Some of the “intersex” fish that have been discovered elsewhere are also believed to have mutated sex organs caused by “endocrine disrupting chemicals” that can mimic estrogens.

In this study, the health concerns identified were found in black scabbardfish, orange roughy, greater forkbeard and other less-well-known species, and included a wide range of degenerative and inflammatory lesions that indicate a host response to pathogens, as well as natural cell turnover. The fish that live in these deep water, sloping regions usually grow slowly, live near the seafloor, and mature at a relatively old age. Some can live to be 100 years old.

Partly because of that longevity, the fish have the capacity to bioaccumulate toxicants, which the researchers said in their report “may be a significant human health issue if those species are destined for human consumption.” Organic pollutants in such species may be 10-17 times higher than those found in fish from the continental shelf, the study noted, with the highest level of contaminants in the deepest-dwelling fish.

However, most of those contaminants migrate to the liver and gonads of such fish, which would make their muscle tissue comparatively less toxic, and “generally not high enough for human health concern,” the researchers wrote.

The corresponding author on this study was Stephen Feist at the Centre for Environment, Fisheries and Aquaculture Science in Weymouth, England.

In the previous research done in the American West, scientists found toxic contamination from pesticides, the burning of fossil fuels, agriculture, industrial operations and other sources, which primarily found their way into high mountain lakes through air pollution. Pesticide pollution, in particular, was pervasive.

Together, the two studies suggest that fish from some of the most remote parts of the planet, from high mountains to deep ocean, may be impacted by toxicants, Kent said.

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Michael Kent, 541-737-8652

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Testicle with egg
Trout testicle with egg

Genetic discovery may offer new avenue of attack against schistosomiasis

CORVALLIS, Ore. – Researchers at Oregon State University have discovered a group of genes in one species of snail that provide a natural resistance to the flatworm parasite that causes schistosomiasis, and opens the door to possible new drugs or ways to break the transmission cycle of this debilitating disease.

Schistosomiasis infects more than 200 million people in more than 70 countries, and is most common in areas with poor sanitation. It can cause chronic, lifelong disability, beginning with gastrointestinal problems and sometimes leading to liver damage, kidney failure, infertility and bladder cancer.

Schistosomisasis, which is native to Africa but has now spread around the world, has been called a neglected global pandemic. Its impact on human health rivals that of malaria.

However, the circular transmission of this complex disease depends upon spending some time as an infection in aquatic snails, where the number of parasites is greatly magnified. Snails may therefore offer a key opportunity to break the cycle of transmission.

The findings about this genetic discovery were just published in PLOS Genetics, by researchers from OSU and the Universite de Perpignan Via Domitia in France. The work was supported by the National Institutes of Health.

“We’ve found a new class of previously unknown genes that appear to control the ability to resist schistosomes,” said Michael Blouin, a professor of integrative biology in the OSU College of Science. “It was found that a dominant genetic allele in this region conveys an eight-fold decrease in the risk of schistosomiasis infection.

“These genes are the type that, in other animal species, help to recognize pathogens and trigger an immune response,” Blouin said. “This is important new information. With further research we’ll learn more about the exact genetics and molecules that are involved as the parasite interacts with the host.”

There are two possible applications of these results that could be pursued in an effort to treat or control this disease, the researchers said. One would be development of new drugs, which could be important - right now only a single medication, praziquantel, exists to help treat the disease. With its increasingly widespread use, resistance to that drug is possible.

Alternatively, researchers might attempt to insert these parasite-resistant genes into the species of snails that most commonly transmit schistosomiasis.

“There are ways to drive new genes into a population,” said Jacob Tennessen, an OSU postdoctoral research associate and lead author on this study.

This is already being tried for some other diseases, the scientists noted, such as in mosquitos that transmit malaria. Modifying snail populations to be resistant is currently not practical, they said, but identifying new genes that control resistance to the parasite is a critical first step.

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Michael Blouin, 541-737-2362

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Resisting schistosomiasis
Schistosomiasis resistance

Trematode eggs
Trematode eggs

Global warming to increase ocean upwelling, but fisheries impact uncertain

CORVALLIS, Ore. – A report to be published Thursday in the journal Nature suggests that global warming may increase upwelling in several ocean current systems around the world by the end of this century, especially at high latitudes, and will cause major changes in marine biodiversity.

Since upwelling of colder, nutrient-rich water is a driving force behind marine productivity, one possibility may be enhancement of some of the world’s most important fisheries.

However, solar heating due to greenhouse warming may also increase the persistence of “stratification,” or the horizontal layering of ocean water of different temperatures. The result could be a warm, near-surface layer and a deep, cold layer.

If this happens to a significant extent, it could increase global hypoxic, or low-oxygen events, decouple upwelling from the supply of nutrient-rich water, and pose a significant threat to the global function of fisheries and marine ecosystems.

The projected increase in upwelling, in other words, appears clear and definitive. But researchers say its biological impact is far less obvious, which is a significant concern.

These upwelling systems cover less than 2 percent of the ocean surface, but contribute 7 percent to global marine primary production, and 20 percent of global fish catches.

“Our modeling indicates that normally weaker upwelling toward the polar ends of upwelling-dominated regions will strengthen,” said Bruce Menge, the Wayne and Gladys Valley Professor of Marine Biology in the College of Science at Oregon State University, and co-author of the report.

“Ordinarily, you would expect that an increase in upwelling would mean an increase in marine coastal productivity, and that might happen,” Menge said.

“However, a thicker and warmer top later, and more stratified ocean waters may put the cold, nutrient-rich waters too deep for upwelling to bring them up, and reduce the ability of upwelling to energize the coastal ocean food web,” he said. “This could have a very negative impact on marine production and fisheries.”

The findings were made by researchers from OSU and Northeastern University, in work supported by that university and the National Science Foundation.

Another possibility, the study concluded, are changes in the frequency or severity of low-oxygen, or “hypoxic” events such as those that have plagued the Pacific Northwest in the past decade. Depending on where the layers of warm and cold water end up, as well as local subsea terrain and currents, the hypoxic events could become either less common or more severe. In a hypoxic event, microbial decay of phytoplankton blooms uses up the available oxygen, causes hypoxia, and often leads to a die-off of fish and other marine organisms.

Among the findings of the study:

  • The change in upwelling may be more pronounced in the Southern Hemisphere, due to the local influences of land masses, coastline, water depth and other issues.
  • Major current systems will be affected off the western coasts of North America, South America, Africa and parts of Europe.
  • The general increase in upwelling is going to be driven by a strengthening of alongshore winds, due to a differential in land and ocean heating.
  • At high, but not low latitudes, the upwelling season will start earlier, last longer and be more intense.
  • At tropical and sub-tropical latitudes, upwelling will become almost a year-round phenomenon.
  • The findings are consistent with different research which shows that coastal upwelling has intensified over the past 60 years.
  • Impacts on the California Current System are expected to be less pronounced because of other climatic forces at work, such as the Pacific Decadal Oscillation, the El Nino-Southern Oscillation, and the North Pacific Gyre Oscillation.

Researchers said that by understanding these climate-mediated “hotspots” in upwelling, and how they will change in the future, it may be possible to better manage productive fisheries and coastal ecosystems around the world.

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Bruce Menge, 541-737-5358

Unwanted impact of antibiotics broader, more complex than previously known

CORVALLIS, Ore. – Researchers at Oregon State University have discovered that antibiotics have an impact on the microorganisms that live in an animal’s gut that’s more broad and complex than previously known.

The findings help to better explain some of the damage these medications can do, and set the stage for new ways to study and offset those impacts.

The work was published online in the journal Gut, in research supported by Oregon State University, the Medical Research Foundation of Oregon and the National Institutes of Health.

Researchers have known for some time that antibiotics can have unwanted side effects, especially in disrupting the natural and beneficial microbiota of the gastrointestinal system. But the new study helps explain in much more detail why that is happening, and also suggests that powerful, long-term antibiotic use can have even more far-reaching effects.

Scientists now suspect that antibiotic use, and especially overuse, can have unwanted effects on everything from the immune system to glucose metabolism, food absorption, obesity, stress and behavior.

The issues are rising in importance, since 40 percent of all adults and 70 percent of all children take one or more antibiotics every year, not to mention their use in billions of food animals. Although when used properly antibiotics can help treat life-threatening bacterial infections, more than 10 percent of people who receive the medications can suffer from adverse side effects.

“Just in the past decade a whole new universe has opened up about the far-reaching effects of antibiotic use, and now we’re exploring it,” said Andrey Morgun, an assistant professor in the OSU College of Pharmacy. “The study of microbiota is just exploding. Nothing we find would surprise me at this point.”

This research used a “cocktail” of four antibiotics frequently given to laboratory animals, and studied the impacts.

“Prior to this most people thought antibiotics only depleted microbiota and diminished several important immune functions that take place in the gut,” Morgun said. “Actually that’s only about one-third of the picture. They also kill intestinal epithelium. Destruction of the intestinal epithelium is important because this is the site of nutrient absorption, part of our immune system and it has other biological functions that play a role in human health.”

The research also found that antibiotics and antibiotic-resistant microbes caused significant changes in mitochondrial function, which in turn can lead to more epithelial cell death. That antibiotics have special impacts on the mitochondria of cells is both important and interesting, said Morgun, who was a co-leader of this study with Dr. Natalia Shulzhenko, a researcher in the OSU College of Veterinary Medicine who has an M.D. from Kharkiv Medical University.

Mitochondria plays a major role in cell signaling, growth and energy production, and for good health they need to function properly.

But the relationship of antibiotics to mitochondria may go back a long way. In evolution, mitochondria descended from bacteria, which were some of the earliest life forms, and different bacteria competed with each other for survival. That an antibiotic would still selectively attack the portion of a cell that most closely resembles bacteria may be a throwback to that ingrained sense of competition and the very evolution of life.

Morgun and Schulzhenko’s research group also found that one of the genes affected by antibiotic treatment is critical to the communication between the host and microbe.

“When the host microbe communication system gets out of balance it can lead to a chain of seemingly unrelated problems,” Morgun said.

Digestive dysfunction is near the top of the list, with antibiotic use linked to such issues as diarrhea and ulcerative colitis. But new research is also finding links to obesity, food absorption, depression, immune function, sepsis, allergies and asthma.

This research also developed a new bioinformatics approach named “transkingdom network interrogation” to studying microbiota, which could help further speed the study of any alterations of host microbiota interactions and antibiotic impact. This could aid the search for new probiotics to help offset antibiotic effects, and conceivably lead to systems that would diagnose a person’s microbiome, identify deficiencies and then address them in a precise and individual way. 

Healthy microbiota may also be another way to address growing problems with antibiotic resistance, Morgun said. Instead of trying to kill the “bad” bacteria causing an illness, a healthy and functioning microbiota may be able to outcompete the unwanted microbes and improve immune function.

Collaborators on this research were from the OSU College of Pharmacy; OSU College of Veterinary Medicine; OSU College of Science; the National Cancer Institute; University of British Columbia; University of Maryland School of Medicine; and the National Institutes of Health.

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Andrey Morgun, 541-737-8047

Amber fossil links earliest grasses, dinosaurs and fungus used to produce LSD

CORVALLIS, Ore. – A perfectly preserved amber fossil from Myanmar has been found that provides evidence of the earliest grass specimen ever discovered – about 100 million years old – and even then it was topped by a fungus similar to ergot, which for eons has been intertwined with animals and humans.

Ergot has played roles as a medicine, a toxin, and a hallucinogen; been implicated in everything from disease epidemics to the Salem witch trials; and more recently provided the hallucinogenic drug LSD.

Apparently both ergot and the grasses that now form most of the diet for the human race evolved together.

And if they already seemed a little scary, imagine a huge sauropod dinosaur that just ate a large portion of this psychotropic fungus, which in other animal species can cause anything from hallucinations to delirium, gangrene, convulsions or the staggers. The fungus, the grasses it lived on and dinosaurs that ate grass co-existed for millions of years.

The findings and analysis of this remarkable fossil were just published online in the journal Palaeodiversity, by researchers from Oregon State University, the USDA Agricultural Research Service and Germany.

“It seems like ergot has been involved with animals and humans almost forever, and now we know that this fungus literally dates back to the earliest evolution of grasses,” said George Poinar, Jr., an internationally recognized expert on the life forms found in amber and a faculty member in the OSU College of Science.

“This is an important discovery that helps us understand the timeline of grass development, which now forms the basis of the human food supply in such crops as corn, rice or wheat,” Poinar said. “But it also shows that this parasitic fungus may have been around almost as long as the grasses themselves, as both a toxin and natural hallucinogen.

“There’s no doubt in my mind that it would have been eaten by sauropod dinosaurs, although we can’t know what exact effect it had on them.”

Amber begins as a tree sap that can flow around small plant and animal forms and permanently preserve them, as it fossilizes into a semi-precious stone. Poinar is a world leader in examining such specimens and using them to learn more about prehistoric ecosystems.

The fungus in this grass specimen, which is now extinct, was named Palaeoclaviceps parasiticus. It’s very similar to the fungus Claviceps, commonly known as ergot. The fossil, taken from amber mines in Myanmar, dates 97-110 million years ago to the early-to-mid Cretaceous, when the land was still dominated by dinosaurs and conifers, but the earliest flowering plants, grasses and small mammals were beginning to evolve. The fossil shows a grass floret tipped by the dark fungus.

Much later in evolution, grasses would become a powerful life form on Earth, creating vast prairies, nourishing herds of animals, and eventually providing for the domestication of range animals and the cultivation of many food crops. The rise of crop agriculture changed the entire development of the human race, and it’s now estimated that grasses compose about 20 percent of global vegetation.

Researchers also noted in their report that “few fungi have had a greater historical impact on society than ergot.”

Some grasses have natural defense mechanisms, and ergot may be one of them, helping to repel herbivores. It’s bitter and not a preferred food to livestock, and it’s still a problem in cereal and grass seed production, as well as pastures and grazing land.

In animal and human history, the fungus has been known to cause delirium, irrational behavior, convulsions, severe pain, gangrenous limbs and death. In cattle it causes a disease called the “Paspalum staggers.” In the Middle Ages it sometimes killed thousands of people during epidemics when ergot-infected rye bread was more common. It’s been used as a medicine to induce abortion or speed labor in pregnant women, and one researcher – whose findings have been disputed – suggested it may have played a role in the Salem witch trials.

More than 1,000 compounds have been extracted or derived from it, some of them valuable drugs. They also included, in the mid-1900s, the powerful psychedelic compound lysergic acid diethylamide, or LSD, that is still being studied and has been widely used as an illegal recreational drug.

Ergot is strange. And a very, very old fossil now makes clear that it’s been around about as long as grass itself.

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George Poinar, Jr., 541-760-7319

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Oldest grass fossil

Grass spikelet with ergot

Deworming programs in animal, human populations may have unwanted impacts

CORVALLIS, Ore. – A study of the effects of worming medications on infectious disease in wildlife herds showed an unexpected and alarming result – although it helped reduce individual deaths from a bovine tuberculosis infection, it hugely increased the potential for spread of the disease to other animals.

The findings, from one of the first field studies ever done on this issue, will be published Friday in the journal Science.

They were contrary to expectations based on laboratory studies, and suggest the possibility that broad use of medical treatments such as this can backfire. They may actually increase the problem with diseases they were meant to reduce.

Both in animals and possibly human disease, treatments that aid an individual could come at the expense of a wider spread of disease in the larger community, the research suggested.

“This study indicates that we need to better understand how some medical treatments affect other health issues, in particular infectious disease,” said Anna Jolles, an epidemiologist at Oregon State University and co-author of the study, along with Vanessa Ezenwa at the University of Georgia.

The research, supported by the National Science Foundation, was done with more than 200 animals in two herds of free-ranging African buffalo in Kruger National Park in South Africa. Half were given deworming medication and the others not.

It was known that infection with parasitic helminth worms can decrease the effective immune response against some infectious diseases, in this case bovine tuberculosis, which is common among these animals. Scientists expected the worming medications to save lives while reducing the risk of infection and disease progression.

They found that deworming treatments did improve the survival of animals infected with bovine tuberculosis – in fact, dewormed animals with tuberculosis survived just as well as TB-free animals. However, deworming did not reduce the risk of new infections, and there was a dramatic eight-fold increase in the number of buffalos that an infected animal could potentially infect – a reference to the “R-nought,” or reproductive multiplier that epidemiologists use to predict the potential for spread of infection in a community.

A buffalo with bovine tuberculosis but no worm treatments has, on average, the potential to infect about one other buffalo. This study found that after worm treatment, a buffalo with this disease had the theoretical potential to infect nine other buffalos. This difference was based on the finding that dewormed buffalo with TB can survive for years, whereas the life expectancy of untreated TB-infected buffalo was much shorter.

These issues are of significant concern not just for animal, but also human health, researchers say.

Helminth worm infections are among the most ubiquitous parasites on Earth, infecting 1 billion people and causing significant losses among both livestock and wildlife. Other studies have linked co-infection with these worms to increased risk of death from both tuberculosis and HIV/AIDS in human patients, largely due to their ability to reduce and otherwise skew the natural immune response to both viral and bacterial infection.

This is a larger problem in the developing world, and some major deworming programs in human populations are already in place due to the range of health concerns posed by the parasites. It’s believed that mass deworming programs may reduce overall deaths from some of the major killers in such areas, such as malaria, tuberculosis and HIV infection.

“These results are pretty alarming,” said Jolles, who is a researcher in both the OSU College of Science and College of Veterinary Medicine.

“We expected deworming effects to be all positive, both for individual buffalo, and in terms of reducing disease spread,” Jolles said. “But what we found is positive effects for individual animals, but potentially much faster disease spread at the population level.”

From these results in buffalo, Jolles said, one should not to jump to conclusions about changing deworming treatments in people. But they do raise questions about large, broad-based public deworming programs.

“We must pay attention to health problems that may increase as a result of the program, as well as problems that we are solving,” she said.

The findings also raise questions about aspects of animal agriculture, Jolles said, especially in developing countries. It may be important to match deworming programs with vaccines for infectious disease and other treatments to ensure that the overall health of the herd is protected.

The potential to actually increase spread of a disease following a health treatment such as deworming may vary widely, Jolles said, with different animal species and different infectious diseases.

More studies are urgently needed to address the primary question raised by this research, the scientists said. On a community level, will large-scale deworming treatments alleviate, or will they exacerbate the health impacts of other, sometimes deadly infections?

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Anna Jolles, 541-737-4719

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African buffalo

African buffalo

OSU marine ecologist chosen as first U.S. Science Envoy for Oceans

WASHINGTON, D.C. – Building on a new commitment to improved marine protection and management, the U.S. Department of State has chosen Jane Lubchenco as the first Science Envoy for the Oceans.

Officials today named the fourth cohort of the U.S. Science Envoy Program, which was begun by President Obama in 2009. For the first time, one of the eminent scientists involved in the initiative has a specific focus on the world’s oceans.

Lubchenco is the University Distinguished Professor of Marine Biology at Oregon State University and former administrator of the National Oceanic and Atmospheric Administration. She is an international expert on marine ecology, environmental science and climate change.

“This new focus on the oceans is a strong statement by the Secretary of State and President Obama about the importance of our oceans to people around the world,” Lubchenco said. “They understand that science-based understanding, policy and management hold the key to a healthy, productive and resilient ocean, people and communities.”

Three other science envoys were also announced to focus on various nations and areas of expertise, including Geraldine Richmond, presidential chair and professor of chemistry at the University of Oregon.

In this program, these “envoys” travel internationally as private citizens, but will also advise and share their insights with the White House, U.S. Department of State and the U.S. science community about science-based collaboration, innovation and economic growth.

Lubchenco said her appointment builds on progress made earlier this year at the Our Ocean Conference led by Secretary of State John Kerry.

Noting that she was “deeply honored to be named to the position,” Lubchenco said she hopes to work with international colleagues to identify opportunities for science-based policies, building scientific capacity and exchanging findings.

“Around the world, the ocean is changing,” Lubchenco said. “Climate change, ocean acidification, overfishing, habitat destruction and pollution are all critical concerns. But we believe it’s possible to identify smart, science-based approaches that can help cope with many of these challenges.”

Science might help transform small-scale fisheries that are essential to the livelihoods and food security of millions of people into more sustainable and profitable fisheries, Lubchenco said. Marine protected areas could more effectively serve as “fish banks” to replenish fisheries, while also protecting habitats and biodiversity. And various steps could be taken to buffer against the forces of climate and other environmental changes.

“We haven’t yet decided on specific projects or regions,” Lubchenco said, “but we’re going to explore all the ways in which science can help create a healthy ocean, healthy people and a prosperous economy.

Lubchenco, who does research in the Department of Integrative Biology of the OSU College of Science, also said the new position will fit well with the Marine Studies Initiative at OSU, and provide opportunities for faculty and students to become more involved in new research and initiatives.

Media Contact: 
Source: 

 Jane Lubchenco, Lubchenco@oregonstate.edu

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