Syndicate content

Archive - Aug 6, 2014

The Insecticides Fipronil and Imidacloprid Reduce Honeybee Mitochondrial Activity

New research published online on August 6, 2014 in Environmental Toxicology and Chemistry addresses the effects of two broad-spectrum systemic insecticides, fipornil and imidacloprid, on honeybees. These insecticides are widely used in agriculture, and the authors conclude that fipronil and imidacloprid are inhibitors of mitochondrial bioenergetics, resulting in depleted cell energy. This action can explain the toxicity of these compounds for honeybees. Scientists are urgently trying to determine the causes of colony collapse disorder and the alarming population declines of honeybees. The cross-pollination services they provide are required by approximately 80 percent of all flowering plants, and 1/3 of all agricultural food production directly depends on bee pollination. As a result, there has been a flurry of research on honeybee parasitic mite infestations, viral diseases, and the direct and indirect impacts of pesticides. The effects of pyrazoles (e.g., fipronil) and neonicotinoids (e.g., imidacloprid) on the nervous system are fairly well documented. Dr. Daniel Nicodemo, professor of ecology and beekeeping at the Universidade Estadual Paulista in Dracena, Brazil, and lead author of the study states, "These insecticides affect the nervous system of pest and beneficial insects, often killing them. Sublethal effects related to insect behavior have been described in other studies; even a few nanograms of active ingredient disturbed the sense of taste, olfactory learning, and motor activity of the bees." A key characteristic of colony collapse disorder is the incapacity of the honeybees to return to their hives, and these disruptions have a direct impact on that ability. In this study, Dr.

Galectin-1 Covers and Protects Malignant Gliomas from Natural Killer Cells

Brain tumors fly under the radar of the body's defense forces by coating their cells with extra amounts of a specific protein, new research shows. Like a stealth fighter jet, the coating means the cells evade detection by the early-warning immune system that should detect and kill them. The stealth approach lets the tumors hide until it's too late for the body to defeat them. The findings, made in mice and rats, show the key role of a protein called galectin-1 (see image) in some of the most dangerous brain tumors, called high-grade malignant gliomas. A research team from the University of Michigan (U-M) Medical School made the discovery and published it online on July 16, 2014 in Cancer Research. In a stunning example of scientific serendipity, the team uncovered galectin-1's role by pursuing a chance finding. They had actually been trying to study how the extra production of galectin-1 by tumor cells affects cancer's ability to grow and spread in the brain. Instead, they found that when they blocked cancer cells from making galectin-1, the tumors were eradicated; they did not grow at all. That's because the "first responders" of the body's immune system – called natural killer or NK cells – spotted the tumor cells almost immediately and killed them. But when the tumor cells made their usual amounts of galectin-1, the immune cells couldn't recognize the cancerous cells as dangerous. That meant that the immune system couldn't trigger the body's "second line of defense," called T cells – until the tumors had grown too large for the body to defeat. Team leader Pedro Lowenstein, M.D., Ph.D., of the U-M Department of Neurosurgery, says the findings open the door to research on the effect of blocking galectin-1 in patients with gliomas.

Finding Lays Groundwork for New Class of Antibiotics to Fight Multi-Drug-Resistant Staph aureus

St. Jude Children’s Research Hospital scientists have discovered an enzyme that regulates production of the toxins that contribute to potentially life-threatening Staphylococcus aureus infections. The study appeared online on July 7, 2014 in PNAS. Researchers also showed that the same enzyme allows Staphylococcus aureus to use fatty acids acquired from the infected individual to make the membrane that bacteria need to grow and flourish. The results provide a promising focus for efforts to develop a much-needed new class of antibiotics to combat staph and other Gram-positive infections. Staphylococcus aureus is the most common cause of staph infections, including methicillin-resistant Staphylococcus aureus (MRSA), the drug-resistant infection that is a growing problem in hospitals. “Staphylococcus aureus is a clear and present danger to patients worldwide,” said corresponding author Charles Rock, Ph.D., a member of the St. Jude Department of Infectious Diseases. “We set out to answer a long-standing question about bacterial membrane biochemistry and discovered a master regulator of the virulence factors that make staph infections so destructive and dangerous. The pathway we identified offers an exciting new target for antibiotic drug development.” Virulence factors include dozens of proteins that bacteria make and secrete. The factors cause many symptoms and infection-related problems, including destruction of cells and tissue, and evasion of the immune system. The enzyme Dr. Rock and his colleagues discovered is fatty acid kinase (FAK). Researchers showed that FAK is formed by the proteins FakA and FakB1 or FakB2. Scientists demonstrated how FakA and FakB work together to replace fatty acids in the bacterial membrane with fatty acids from the person infected.

Discovery about Wound Healing Key to Understanding Cell Movement

Research by a civil engineer from the University of Waterloo in Canada is helping shed light on the way wounds heal and may someday have implications for understanding how cancer spreads, as well as why certain birth defects occur. Professor Wayne Brodland is developing computational models for studying the mechanical interactions between cells. In this project, he worked with a team of international researchers who found that the way wounds knit together is more complex than we thought. The results were published online on August 3, 2014 in Nature Physics. "When people think of civil engineering, they probably think of bridges and roads, not the human body," said Professor Brodland. "Like a number of my colleagues, I study structures, but ones that happen to be very small, and under certain conditions they cause cells to move. The models we build allow us to replicate these movements and figure out how they are driven." When you cut yourself, a scar remains, but not so in the cells the team studied. The researchers found that an injury closes by cells crawling to the site and by contraction of a drawstring-like structure that forms along the wound edge. They were surprised to find that the drawstring works fine even when it contains naturally occurring breaks. This knowledge could be the first step on a long road towards making real progress in addressing some major health challenges. "The work is important because it helps us to understand how cells move. We hope that someday this knowledge will help us to eliminate malformation birth defects, such as spina bifida, and stop cancer cells from spreading," said Professor Brodland. The research team was composed of ten researchers from Spain, France, Singapore, and Canada. Professor Brodland is one of the paper's two Canadian co-authors.

Reported Cure of Rheumatoid Arthritis in Mice

Rheumatoid arthritis is a condition that causes painful inflammation of several joints in the body. The joint capsule becomes swollen, and the disease can also destroy cartilage and bone as it progresses. Rheumatoid arthritis affects 0.5% to 1% of the world’s population. Up to this point, doctors have used various drugs to slow or stop the progression of the disease. But now, ETH Zurich researchers in Switzerland have developed a therapy that takes the treatment of rheumatoid arthritis in mice to a new level: after receiving the medication, researchers consider the animals to be fully cured. The drug is a biotechnologically produced active substance consisting of two fused components. One component is the body’s own immune messenger interleukin 4 (IL-4) (image); previous studies have shown that this messenger protects mice with rheumatoid arthritis against cartilage and bone damage. ETH scientists have coupled an antibody to IL-4 that, based on the key-lock principle, binds to a form of a protein that is found only in inflamed tissue in certain diseases (and in tumor tissue). “As a result of combination with the antibody, IL-4 reaches the site of the disease when the fusion molecule is injected into the body,” says pharmacist Dr. Teresa Hemmerle, who has just completed her dissertation in the group of Dr. Dario Neri, a professor at the Institute of Pharmaceutical Sciences. Together with Fabia Doll, also a Ph.D. pharmacist at ETH, she is the lead author of the study that appeared online on August 4, 2014 in PNAS. “It allows us to concentrate the active substance at the site of the disease. The concentration in the rest of the body is minimal, which reduces side-effects,” she says.

24 New Species Described in Carabid Beetle Tribe Lachnophorini

An extensive study by Smithsonian scientists presents a synopsis of the carabid beetle tribe Lachnophorini. The research describes a new genus and a remarkable 24 new species added to the tribe. The study was published online on August 1, 2014 in the open-access journal ZooKeys. Beetles from the family Carabidae, commonly known as ground beetles, are a large, cosmopolitan group, with more than 40,000 species worldwide. Carabid beetles range in size from 0.6 mm to 90.2 mm and occur in nature in several fractal universes influencing life therein as predators, ectoparasitoids, seed eaters, and even fungal mycelia feeders in a multitude of ways. Understanding the impact of this beetle family's importance across a multidimensional landscape in a cascade of fractal universes is our biodiversity challenge for the 21st century for one of insects' most diverse families. "For a fairly large and diverse Tribe of Carabidae with markedly interesting body forms and divergent ways of life, the Lachnophorini have all but been largely ignored by carabidologists until now. This new study establishes the groundwork for more refined studies aiming for a better understanding of the diversity of the species and the evolution of the tribe in order to have a finer awareness of the next smaller fractal universe for the Carabidae family, if we are truly to understand it," explains one of the authors Laura Zamorano, research student at the National Museum of Natural History, Smithsonian Institution. This research is the beginning of a series of steps towards the provision of taxonomic relationships of carabid beetles. For the near future, the path forward to be followed will lead to an attempt, using morphological and molecular attributes, to provide a firm basis for firm classification.