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Hothorn L.A.,Leibniz University of Hanover | Hothorn L.A.,Scripps Research Institute | Djira G.D.,SDSU
Pharmaceutical Statistics | Year: 2011

Under certain conditions, many multiple contrast tests based on the difference of treatment means can also be conveniently expressed in terms of ratios. In this paper, a Williams test for trend is defined as ratios-to-control for ease of interpretation and to obtain directly comparable confidence intervals. Simultaneous confidence intervals for percentages are particularly helpful for interpretations in the case of multiple endpoints. Methods for constructing simultaneous confidence intervals are discussed under both homogeneous and heterogeneous error variances. This approach is available in the R extension package mratios. The proposed method is used to test for trend in an immunotoxicity study with several endpoints as an example. © 2010 John Wiley & Sons, Ltd. Source

Wood C.,SDSU | Rosentrater K.A.,Iowa State University | Muthukumarappan K.,South Dakota State University
Industrial Crops and Products | Year: 2014

The need for new value-added applications for ethanol coproducts grows as the U.S. ethanol industry continues to expand. Distillers dried grains with solubles (DDGS), corn gluten meal (CGM), and corn gluten feed (CGF) are the primary coproducts of ethanol manufacturing and are mainly utilized as animal feed. This study examined the use of pyrolysis to extract value from these grains. Characterization of the resulting bio-oil and bio-char included mass density, thermal conductivity, thermal diffusivity, apparent viscosity, kinematic viscosity, and energy content. The bio-oils produced from these ethanol coproducts require some changes to be used commercially. The tar present in the crude bio-oils caused them to have densities greater than one, and caused the oil viscosity to be shear thinning. The pH of these bio-oils is less acidic and thus more favorable than other bio-oils which could be due to the differences in the feedstock composition. © 2014 Elsevier B.V. Source

News Article
Site: http://phys.org/biology-news/

SDSU investigators found that flies with a double-mutation in their myosin protein had better protein function than those with a single mutation. Credit: Mr. checker/Wikimedia Commons Two wrongs don't make a right, but in the case of genetic mutations, having two mutations in the same gene could be better than having either one individually. Recent research by biologists at San Diego State University found that two separate genetic modifications each greatly reduced the function of the myosin muscle protein in fruit flies, but flies with both mutations had nearly three-quarters of the protein function restored. The findings are important for researchers looking to better understand and treat heart muscle disease in humans. Myosin is a motor protein involved in muscle contraction. The proper functioning of this protein depends on a series of chemical bonds that hold the protein in its proper configuration. Mutating the protein to destroy some of these bonds can cause the protein to lose some or all of its function, leading to abnormal muscle contraction in the organism. Earlier studies had suggested that within the myosin protein, the interaction between two amino acid subunits called E497 and R712 is charge-dependent. In other words, in order to normally function, a negative charge on one amino acid interacts with a positive charge on the other. In humans, mutations in either of these amino acids can result in hypertrophic cardiomyopathy, a common form of inherited heart muscle disease. In a recent study, investigators at SDSU looked further into how exactly disrupting the charges of these amino acids might lead to muscle defects. SDSU biologist Sanford Bernstein and colleagues experimented with fruit flies with genetically modified proteins in the flies' flight muscles to see what effects that would have on the proteins' functioning. The researchers bred two versions of fruit flies in which either the fly version of the E497 or the R712 myosin protein amino acids were mutated by having their charges reversed. Those flies lost their flight ability completely. Using a combination of biochemical techniques, the researchers found that the myosin proteins were about five times less active in these flies. A third line of genetically modified flies had the charges reversed in both E497 and R712 myosin protein amino acids. These flies still couldn't fly, but the researchers found that the proteins were about 73-percent as active as those in normal, unmodified flies—a vast improvement over having either single mutation by itself. Interestingly, heterozygous flies (those with copies of both normally functioning and genetically modified genes) in the study did manage to fly when they were young. However, this occurred only for the double-mutant. Overall, the double-mutation restored most of the protein activity that was lost in the other two mutant lines, demonstrating that both amino acids need to interact in a charge-dependent manner in order for normal muscle protein function to occur. The researchers published their results earlier this month in the Journal of Biological Chemistry. Because the myosin protein modified in the flies is so similar to the one known to be involved in some human cardiomyopathy, and since the same amino acids are affected, Bernstein said that a similarly dysfunctional process probably underlies the disease caused by mutations in these specific amino acids in humans. "In humans, it's a different type of mutation, but it's one that we predict is disruptive to normal interaction within the protein, resulting in decreased or possibly increased myosin function," he said. For that reason, researchers can further study these proteins in flies to learn more about the disease. Bernstein said that the team's results suggest that the abnormal function in human heart muscle cells is largely a result of structural failings in the myosin protein that lead to biochemical dysfunction and an unsuccessful attempt to compensate for these defects, resulting in abnormal heart structure and function. What's more, the findings point to the potential for drugs that can modify myosin function to overcome connection errors within abnormally charged myosin proteins, which might improve functioning in human heart muscle cells. More information: William A. Kronert et al. A Failure to Communicate: Myosin Residues Involved in Hypertrophic Cardiomyopathy Affect Inter-Domain Interaction, Journal of Biological Chemistry (2015). DOI: 10.1074/jbc.M115.681874

News Article | November 11, 2015
Site: http://www.techtimes.com/rss/sections/science.xml

Can beauty be quantified? A study revealed that scientists can measure coral reef health through an analysis of the aesthetic quality of reefs or how beautiful they look. Art historians and philosophers from all over the world and from different eras have been looking for ubiquitous and valid criteria that can measure ugliness and beauty. Now, a multidisciplinary team of experts was able to develop a new computational method that can assess what people regard as aesthetically pleasing. Their first application is the assessment of coral reefs. The study, which was issued in the journal[pdf] Peerj, evaluated images of coral reefs and 109 aesthetic features present in the images. These features included relative color, size and location of noticeable objects in the image, as well as color intensity, diversity and texture of the image. Through specifically-designed software, researchers analyzed about 2,000 images of coral reefs and compared them to the customary monitoring procedure known as the National Center for Ecological Analysis and Synthesis (NCEAS) score. The NCEAS score describes the increasing impact of humans on reefs. Researchers then found links between the scores of random images of coral reefs and their corresponding reef ecosystem. Andreas Haas, the study's lead author and a postdoctoral scholar from San Diego State University, said their findings suggest that how people perceive beauty is well-aligned with thriving and healthy ecosystems. Haas explained that the perception of beauty is not entirely subjective, and that it is affected by natural components that show degraded or healthy conditions of an object. He added that measuring the visual features of reef ecosystems is a cost-effective technique that targets their socioeconomic value which is their natural beauty. Sue Sargent, a marine biologist, said previous methods for coral reef health assessment relied on researchers who were highly-trained for observation, but now that a new method has been developed, ordinary citizens could also perform reef monitoring through their computers. It could free up important research funding, she said. "Many animals live in and around coral reefs, so it's crucial that we protect them from further harm," added Sargent. The study is a collaborative effort between SDSU, the Getty Research Institute, and the Scripps Institution of Oceanography, Caribbean Research and Management of Biodiversity (CARMABI), the Université de Paris-Saclay, the College of Charleston, and the University of Amsterdam. Meanwhile, anyone can assess the aesthetic score of images by uploading them on a website created by the researchers.

News Article
Site: http://phys.org/biology-news/

In this electron micrograph of bacteriophages attached to a bacterial cell, the viruses are the size and shape of coliphage T1. In the microscopic life that thrives around coral reefs, San Diego State University researchers have discovered an interplay between viruses and microbes that defies conventional wisdom. As the density of microbes rises in an ecosystem, the number of viruses infecting those microbes rises with it. It has generally been assumed that this growing population of viruses, in turn, kills more and more microbes, keeping the microbial population in check. It's a model known as "kill-the-winner"—the winners being the blooming microbial cells and the killers being the viruses (mostly bacteria-killing viruses known as bacteriophages) that infect them. However, a recent study of virus-host dynamics near coral reefs led by SDSU virologists suggests that, under certain conditions, viruses can change their infection strategy. As potential host microbes become more numerous, some viruses forego rapid replication and opt instead to reside peaceably inside their host, thereby reducing their the viruses' numbers. In a study published today in the journal Nature, the researchers refer to this alternative model as "piggyback-the-winner," and it could have implications for phage-based medicine and ecosystem resilience in the face of environmental disturbances that promote microbial blooms. Microbial population explosions can take many forms—algal blooms in the ocean and in lakes, fungal blights in soil and bacterial infection in humans are just a few examples—and how viruses respond to this rapid microbial growth has long interested ecologists. Many viruses can make the switch between rapid replication and dormant coexistence. For decades, most researchers have assumed that during microbial population booms, their viruses take advantage of the opportunity to multiply by killing the abundant microbial winners. "Kill-the-winner seems to make sense," said Ben Knowles, a viral ecologist at SDSU and the study's lead author. "The logic behind it has been around for a while. The reasoning is very seductive." Knowles, along with the study's other lead author, SDSU postdoctoral researcher Cynthia Silveira, and an international team of collaborators with expertise ranging from mathematics, physics and statistics to ecology and molecular biology, decided to put this model to the test. They collected samples of microbe-rich seawater near coral reefs in both the Pacific and Atlantic Oceans. Then, using a combination of microscopic and genomic techniques, they analyzed those samples for the abundance and nature of both microbes and the viruses that infect them. Under the kill-the-winner model, researchers would expect to find more viruses per microbe in samples with a high microbial density and growth rates. What Knowles and his team found, however, was just the opposite: As microbial abundance increased, the virus-to-microbe ratio decreased significantly. Next, Knowles and his team ran an experiment in which they incubated seawater from a pristine coral reef location and from Mission Bay in San Diego for several days, during which they monitored the viral and microbial abundance. The results matched their field sampling, with virus numbers staying relatively low even as microbial populations bloomed. Why weren't the viruses exploiting the increasing population of hosts by infecting them and multiplying rapidly? Why weren't they killing the winner? Exploring this phenomenon further, the researchers used metagenomic analysis to determine whether the viruses in the sample showed virulent, predatory traits or the hallmarks of non-predatory lifestyles. Intriguingly, they found that in samples with a higher microbe count, viral communities became less virulent. Instead of multiplying and killing off their booming host population, more of the viruses instead integrate themselves into their host. The viruses replicate more slowly, but they also avoid competing with other viruses and having to navigate with the host's own immunity defenses. This piggyback-the-winner model better explains virus -host dynamics during periods of fast microbial growth than the established kill-the-winner model, the researchers said. "When you have a fast-growing host, if you're a virus, you profit more from integration," Knowles said. "It's just intelligent parasitism." A better understanding of these dynamics holds promise for improving human health. For example, specially targeted phages have been suggested as a possible therapy for conditions like cystic fibrosis, which is caused by frequent bacterial lung infections. This discovery also could help improve marine ecologists' understanding of the microbiological forces that influence coral reef health. Explore further: Viruses within the ocean floor comprise the greatest fraction  of the deep biosphere More information: B. Knowles et al. Lytic to temperate switching of viral communities, Nature (2016). DOI: 10.1038/nature17193

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