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Archive - Feb 25, 2015

Emulsifiers in Food May Upset Gut Microbiome and Contribute to Rising Incidences of Inflammatory Bowel Disease and Metabolic Syndrome

Emulsifiers, which are added to most processed foods to aid texture and extend shelf life, can alter the gut microbiota composition and localization to induce intestinal inflammation that promotes the development of inflammatory bowel disease (IBD) and metabolic syndrome, new research shows. The research, published online on Februayr 25, 2015 in Nature, was led by Georgia State University Institute for Biomedical Sciences researchers Dr. Benoit Chassaing and Dr. Andrew T. Gewirtz, and included contributions from Emory University, Cornell University, and Bar-Ilan University in Israel. The Nature article is titled “Dietary Emulsifiers Impact the Mouse Gut Microbiota Promoting Colitis and Metabolic Syndrome.” IBD, which includes Crohn's disease and ulcerative colitis, afflicts millions of people and is often severe and debilitating. Metabolic syndrome is a group of very common, obesity-related disorders that can lead to type 2 diabetes and cardiovascular and/or liver diseases. Incidences of IBD and metabolic syndrome have been markedly increasing since the mid-20th century. The term "gut microbiota" refers to the diverse population of 100 trillion bacteria that inhabits the intestinal tract. Gut microbiota are disturbed in IBD and in metabolic syndrome. The findings of Dr. Chassaing and Dr. Gewirtz suggest that emulsifiers might be partially responsible for these disturbances and for the increased incidences of these diseases. "A key feature of these modern plagues is alteration of the gut microbiota in a manner that promotes inflammation," says Dr. Gewirtz. "The dramatic increase in these diseases has occurred despite consistent human genetics, suggesting a pivotal role for an environmental factor," says Dr.Chassaing.

Human-Specific Enhancer DNA Segment Increases Brain Volume in Developing Mouse Embryo by 12% Relative to Effect of Orthologous Chimp Enhancer DNA Segment in Same System; Size Increase Seen in Developing Neocortex, the Center for Language and Reasoning

The size of the human brain expanded dramatically during the course of evolution, giving humans unique capabilities such as the abilities to use abstract language and do complex math. But how did the human brain get larger than that of our closest living relative, the chimpanzee, if almost all of our genes are the same? Duke scientists have shown that it is possible to pick out key changes in the genetic code between chimpanzees and humans and then visualize their respective contributions of those changes to early brain development by using mouse embryos. The team found that humans are equipped with tiny differences in a particular regulator of gene activity, called HARE5, that, when introduced into a mouse embryo, led to a 12% bigger brain than the brain that developed in mouse embryos treated with the corresponding HARE5 sequence from chimpanzees. These findings, which were published online on February 19, 2015 in Current Biology, may lend insight, not only into what makes the human brain special, but also to why people get some diseases, such as autism and Alzheimer’s disease, whereas chimpanzees do not. “I think we’ve just scratched the surface, in terms of what we can gain from this sort of study,” said Debra Silver, Ph.D., an Assistant Professor of Molecular Genetics and Microbiology in the Duke University Medical School and an Investigator in the Duke Institute for Brain Sciences. “There are some other really compelling candidates [in addition to HARE5] that we found that may also lead us to a better understanding of the uniqueness of the human brain.” The Current Biology article is titled “Human-Chimpanzee Differences in a FZD8 Enhancer Alter Cell-Cycle Dynamics in the Developing Neocortex.”

Deadliest Malaria Parasite Uses Anti-Sense Long Noncoding RNAs (lncRNAs) to Specifically Regulate and Periodically Switch Expression of Single Members of Its ~50-var-Gene-Family to Avoid Detection by Human Immune System

Up to one million people, mainly pregnant woman and young children, are killed each year by the Plasmodium falciparum parasite, which causes the most devastating form of human malaria. Now, researchers at the Hebrew University of Jerusalem have revealed the genetic trickery this deadly parasite deploys to escape attack by the human immune system. The parasite is known to replicate within the circulating blood of infected individuals and modify the surface of infected red blood cells. Its virulence comes from its impressive ability to hide from the immune system by selectively changing which surface proteins it displays. This sophisticated game of hide-and-seek, which involves continually alternating the foreign molecules, called antigens, that can trigger an immune response, is called antigenic variation. Previous research has shown that the antigens the parasite selectively expresses, and which are displayed at the surfaces of infected red blood cells, are encoded by members of a gene family named var. The multi-gene var family codes for approximately 50 variant adhesive proteins expressed in a mutually exclusive manner at the surface of infected red blood cells. The parasite tightly regulates the expression of these var genes so that only one is expressed at any given time, while the rest of the family is maintained as silent. Understanding this complex mechanism is essential to understanding how the deadly Plasmodium falciparum parasite evades the human immune system. It is also more broadly important to science because the process by which cells can express a single gene while keeping alternative genes silent is one of the unsolved mysteries in the field of eukaryotic gene expression.

High-Altitude Mountain Chickadees Are Better Problem-Solvers Than Lower-Altitude Mountain Chickadees

Living on harsh, unforgiving icy mountains can make one mentally sharper, and this applies to birds as well. That's what Dr. Dovid Kozlovsky and his colleagues at the University of Nevada in the United States believe after finding that mountain chickadees (Poecile gambeli) that live at higher altitudes are better problem solvers than birds of the same species hailing from lower regions. Their new findings were published online on February 17, 2015 in Behavioral Ecology and Sociobiology. The article is titled “Problem Solving Ability and Response to Novelty in Mountain Chickadees (Poecile gambeli) from Different Elevations.” Mountain chickadees, a North American bird in the tit family, store away food for later occasions. These birds are found at different elevations, where varying winter conditions are experienced. Previous research showed that mountain chickadees living at harsher high elevations have bigger hippocampi, a part of the brain that plays an important role in memory and spatial navigation. These high-elevation chickadees also have far superior spatial memory relative to lower-elevation chickadees. This helps the high-altitude chickadee to be better at remembering where they hid food away. Animals living in challenging or unpredictable environments such as deserts or snowy mountain peaks are generally thought to have enhanced mental abilities. These include being better able to solve problems and not shying away from inspecting new things. To understand if this is true for mountain chickadees, Dr. Kozlovsky and his colleagues caught 24 young birds, in the Sagehen Experimental Forest in California, that had not yet experienced a winter. Twelve birds were caught at a site approximately 1,800 meters above sea level, while another dozen were captured at 2,400 meters above sea level.

Key Genes for Establishment of Symbiosis Between Ectomycorrhiza Fungi (Forest Mushrooms) and Tree Roots Evolved independently and Repeatedly Over Evolutionary Time in Different Fungal Lines

The life style of ectomycorrhiza fungi is some 100 million years younger than the life style of their ancestors within the white and brown rot fungi. The key genome adaptation enabling fungi to associate with roots in order to establish a symbiosis evolved independently and repeatedly in different lines of fungi over time. This conclusion was drawn by an international team of researchers who performed the first comprehensive comparative phylogenomic analysis of mycorrhiza fungi. The results of this study were published online on February 24, 2015 in an open-access article in Nature Genetics. The article was titled “Convergent Losses of Decay Mechanisms and Rapid Turnover of Symbiosis Genes in Mycorrhizal Mutualists.” The reported analysis provides crucial information on how the symbiosis between fungi and trees evolved. This information will enable scientists to improve their prediction of the reaction of mycorrhizal communities to environmental modifications such as changes in forest management or climate. Three scientists of the Helmholtz Centre for Environmental Research (UFZ) contributed to this discovery that also received support from the German Centre for Integrative Biodiversity Research (iDiv) Halle-Jena-Leipzig. Ectomycorrhiza fungi live on the roots of trees, to which these fungi deliver soil minerals, in exchange for sugar produced by the trees via photosynthesis. Almost all land plants establish similar kinds exchange relationships with fungal communities in their root vicinity. Mycorrhiza soil fungi play an important role in terrestrial ecosystems because they regulate the below-ground cycling of matter and carbon. In addition, they link different plants together by a common mycelial network that promotes exchanges within the vegetation.