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Archive - Aug 2014

August 16th

Beetle’s Scales Are Whitest, Most Efficient Light-Scattering Biological Material Known, Could Prove Basis for Brighter, Whiter Coatings and Materials

The physical properties of the ultra-white scales on certain species of beetle could be used to make whiter paper, plastics, and paints, while using far less material than is used in current manufacturing methods. The Cyphochilus beetle (image), which is native to South-East Asia, is whiter than paper, thanks to ultra-thin scales which cover its body. A new investigation of the optical properties of these scales has shown that they are able to scatter light more efficiently than any other biological tissue known, which is how they are able to achieve such a bright whiteness. The findings were published online on August 15, 2014 in an open-access article in Scientific Reports. Animals produce colors for several purposes, from camouflage to communication, to mating and thermoregulation. Bright colors are usually produced using pigments, which absorb certain wavelengths of light and reflect others, which our eyes then perceive as color. To appear as white, however, a tissue needs to reflect all wavelengths of light with the same efficiency. The ultra-white Cyphochilus and L. Stigmabeetles produce this coloration by exploiting the geometry of a dense complex network of chitin – a molecule similar in structure to cellulose, which is found throughout nature, including in the shells of molluscs, the exoskeletons of insects, and the cell walls of fungi. The chitin filaments are just a few billionths of a meter thick, and on their own are not particularly good at reflecting light. The current research, a collaboration between the University of Cambridge and the European Laboratory for Non-Linear Spectroscopy in Italy, has shown that the beetles have optimized their internal structure in order to produce maximum white with minimum material, like a painter who needs to whiten a wall with a very small quantity of paint.

Gut Bacteria May Rule Human Eating Behavior and Dietary Choices

It sounds like science fiction, but it seems that bacteria within us — which outnumber our own cells by approximately 100-fold — may very well be affecting both our cravings and our moods to get us to eat what they want, and often are driving us toward obesity. In an article published online on August 7, 2014 in the journal BioEssays, researchers from the University of California-San Francisco, (UCSF), Arizona State University, and the University of New Mexico concluded from a review of the recent scientific literature that microbes influence human eating behavior and dietary choices to favor consumption of the particular nutrients the microbes grow best on, rather than simply passively living off whatever nutrients humans choose to send their way. Bacterial species vary in the nutrients they need. Some prefer fat, and others sugar, for instance. But they not only vie with each other for food and to retain a niche within their ecosystem — our digestive tracts — they also often have different aims than we do when it comes to our own actions, according to senior author Athena Aktipis, Ph.D., co-founder of the Center for Evolution and Cancer with the Helen Diller Family Comprehensive Cancer Center at UCSF. While it is unclear exactly how this occurs, the authors believe this diverse community of microbes, collectively known as the gut microbiome, may influence our decisions by releasing signaling molecules into our gut. Because the gut is linked to the immune system, the endocrine system, and the nervous system, those signals could influence our physiologic and behavioral responses. "Bacteria within the gut are manipulative," said Carlo Maley, Ph.D., director of the UCSF Center for Evolution and Cancer and the corresponding author on the BioEssays paper.

Prestigious Journal Features Major Article on Preterm Labor

The August 15, 2014 issue of the prestigious journal Science features a major article about the most important problem in obstetrics: preterm labor. The article, "Preterm Labor: One Syndrome, Many Causes," delivers a powerful message: preterm birth is not one condition, but many, and provides a framework for meeting this challenge. "There are 15 million preterm babies born annually, and the condition affects 5 percent to 15 percent of all pregnancies, with the highest rates in North America and Africa. Prematurity is the leading cause of infant death up to age 1and the second-leading cause of childhood death before the age of 5," said Roberto Romero, M.D., D.Med.Sci., chief of the Perinatology Research Branch (PRB) of the Eunice Kennedy Shriver National Institute of Child Health and Human Development located at Wayne State University (WSU) and the Detroit Medical Center (DMC). "We have made progress by identifying the causes of premature labor, and now we propose that it is possible to reframe the problem and make it tractable." A common belief is that preterm labor is merely labor that starts too soon. This perception derives from the fact that labor, whether term or preterm, has the same features – increased uterine contractility, opening of the cervix, and rupture of the membranes. "However," Dr. Romero said, "the fundamental difference is that normal labor at term occurs when the uterus and placenta cannot continue to support the growth of the fetus within the womb. In contrast, preterm labor results from several disease states." Dr. Romero considers premature labor a syndrome – a collection of syndromes and signs – caused by multiple disease processes. A typical example of these disease processes is a "silent" intra-amniotic infection.

Depression Associated with Parkinson’s Disease and Undertreated

Depression is known to be a common symptom of Parkinson’s disease, but remains untreated for many patients, according to a new study by Northwestern Medicine investigators in collaboration with the National Parkinson’s Foundation (NPF). In fact, depression is the most prevalent non-motor symptom of Parkinson’s, a chronic neurodegenerative disorder typically associated with movement dysfunction. This fact is especially relevant now in light of the recent suicide of American comedian Robin Williams (image), who was reported to have been recently diagnosed with the early stages of Parkinson’s disease, while at the same time suffering from depression and anxiety. “We confirmed suspicion that depression is a very common symptom in Parkinson’s disease. Nearly a quarter of the people in the study reported symptoms consistent with depression,” said Danny Bega, M.D., 2014 graduate medical education (GME), instructor in the Ken and Ruth Davee Department of Neurology and first author of the study. “This is important because previous research has determined that depression is a major determinant of overall quality of life.” Using the neuropsychiatric symptoms’ (NPS’s) patient database, the investigators looked at records of more than 7,000 people with Parkinson’s disease. Among those with high levels of depressive symptoms, only one-third had been prescribed antidepressants before the study began, and even fewer saw social workers or mental health professionals for counseling. The investigators then focused their analysis on the remaining two-thirds of patients with depressive symptoms who were not receiving treatment at the start of the study. Throughout a year of observation, fewer than 10 percent of them received prescriptions for antidepressants or referrals to counseling.

Study Suggests Broad Utility of Sequence-Related Amplified Polymorphism (SRAP) Markers

Today, many ecological and evolutionary studies depend on a wide range of molecular tools to infer phylogenetic relationships, uncover population structure within species, and track quantitative traits. Agricultural studies use these same tools to improve crop yield and increase resistance to pests and disease. However, many of these methods—such as amplified fragment length polymorphisms (AFLP), inter-simple sequence repeats (ISSR), and random amplified polymorphic DNA (RAPD)—have technical limitations. These include issues of reproducibility, ambiguity in determining homology, and significant demands on both cost and time for researchers. Sequence-related amplified polymorphism (SRAP) markers show promise as an alternative to traditional markers as they have proven to be highly variable and less technically demanding to obtain and use. This recently developed dominant marker technique produces genome-wide fragments and has been used primarily in studies aimed at crop development. Previous studies have utilized this method to identify pathogen-resistant markers and better understand the genetic basis of fruit and flower form and structure, as well as flowering and fruiting times. In a new, open-access publication in the July 2014 issue of Applications in Plant Sciences, researchers at Ohio State University have made a case for the use of these markers across a broad range of research fields including plant systematics, biogeography, conservation, and ecology. "These markers exhibit variation useful for uncovering genetic structure at a variety of taxonomic levels, constructing linkage maps, and have proven valuable for the improvement of agronomic crops," explains Dr. Daniel Robarts, lead author of the study. Dr.

August 15th

Anti-EphA3 Antibody Has Anti-Tumor Effects Against Solid Tumors and Blood Cancers

An international team of scientists has shown that an antibody against the protein EphA3, found in the micro-environment of solid cancers, has anti-tumor effects. As EphA3 (see image) is present in normal organs only during embryonic development, but is expressed in blood cancers and in solid tumors, this antibody-based approach may be a suitable candidate treatment for solid tumors. The researchers from Monash University and Ludwig Cancer Research, in Australia, and KaloBios Pharmaceuticals, in the US, have had their findings published in the August 15, 2014 issue of Cancer Research The team, led jointly by the late Professor Martin Lackmann, from the School of Biomedical Sciences at Monash; and Professor Andrew Scott, from Ludwig Cancer Research, has found that even if tumor cells do not have this molecule they can thrive by recruiting and taking advantage of supporting EphA3-containing cells in the tumor micro-environment. First author, Dr. Mary Vail, Monash Department of Biochemistry and Molecular Biology said: “The tumor cells send out signals to the surrounding area and say: ‘We need a blood supply and a foundation upon which to spread’. We have shown that EphA3-expressing stromal stem cells, which are produced by the bone marrow, form cells that support and create blood vessels in tumors,” Dr. Vail said. Professor Andrew Scott’s team at Ludwig introduced human prostate cancer cells into a mouse model to mimic disease progression in humans. EphA3 was found in stromal cells and blood vessels surrounding the tumor. The scientists also observed that treatment with an antibody against EphA3 (chIIIA4) significantly slowed tumor growth. The antibody damaged tumor blood vessels and disrupted the stromal micro-environment, and cancer cells died because their ‘life-support’ was compromised.

Review Bolsters Specific Theory of Echolocation in Bats, Suggests Improvements in Sonar and Radar Technologies

Amid a neuroscience debate about how people and animals focus on distinct objects within cluttered scenes, some of the newest and best evidence comes from the way bats “see” with their ears, according to a new paper in the August 15, 2014 issue of the Journal of Experimental Biology. In fact, the perception process in question could be used to improve sonar and radar technology. Bats demonstrate remarkable skill in tracking targets such as bugs through the trees in the dark of night. Dr. James Simmons, professor of neuroscience at Brown University, the review paper’s author, has long sought to explain how they do that. It turns out that experiments in Dr. Simmons’ lab point to the “temporal binding hypothesis” as an explanation. The hypothesis proposes that people and animals focus on objects versus the background when a set of neurons in the brain attuned to features of an object all respond in synchrony, as if shouting in unison, “Yes, look at that!” When the neurons do not respond together to an object, the hypothesis predicts, an object is relegated to the perceptual background. Because bats have an especially acute need to track prey through crowded scenes, albeit with echolocation rather than vision, they have evolved to become an ideal testbed for the hypothesis. “Sometimes the most critical questions about systems in biology that relate to humans are best approached by using an animal species whose lifestyle requires that the system in question be exaggerated in some functional sense so its qualities are more obvious,” said Dr. Simmons, who plans to discuss the research at the 2014 Cold Spring Harbor Asia Conference the week of September 15, 2014 in Suzhou, China. Here’s how he’s determined over the years that temporal binding works in a bat.

August 14th

New Techniques Offer Insight into Cholesterol

With new advanced techniques developed by the Copenhagen Center for Glycomics at the University of Copenhagen, it is possible to study cells in greater detail than ever before. The findings described below have just been published in the June 20, 2014 issue of the Journal of Biological Chemistry and may, in the long term, improve the treatment of high cholesterol. Researchers from the Copenhagen Center for Glycomics at the University of Copenhagen have studied an important receptor protein called LDLR (low-density lipoprotein receptor) (see image) using new, ground-breaking techniques. The protein plays an important role in the absorption of the so-called “bad” cholesterol, LDL (low-density lipoprotein). The key to major discoveries within the fields of health and diseases is not just hidden in the human DNA code. The proteins encoded by the genes also play an important role, not least the attached sugar chains which give the proteins an identity and handle important functions in the human organism. Here, the researchers have studied how LDLR is decorated with sugar molecules, so-called glycosylation modifications. "We have not previously had a simple method for studying where glycosylation modifications are located on proteins in the body, because the sugars are very complicated and appear in different combinations. By removing the Cosmc protein, which is necessary for extending the sugar modifications, we have created cells with simplified glycosylations, which we call SimpleCells. The technique has enabled us to see 20 times as many sugar modifications on our proteins as were previously known," says Nis Borbye Pedersen, Ph.D., formerly postdoc at the Copenhagen Center for Glycomics, now postdoc in the Department of Biology, University of Copenhagen.

How Aspirin May Work to Reduce Female Breast Cancer Deaths

Researchers have discovered that women who had been prescribed aspirin regularly before being diagnosed with breast cancer are less likely to have cancer that spread to the lymph-nodes than women who were not on prescription aspirin. These women are also less likely to die from their breast cancer. The study of Irish patients funded by the Irish Health Research Board and Irish Cancer Society and published by the American Association for Cancer Research in the August 1, 2014 issue of Cancer Research, analyses records from the National Cancer Registry Ireland (NCRI), and prescription data from the General Medical Service (GMS) pharmacy claims database. "Our findings suggest that aspirin could play a role in reducing mortality from breast cancer by preventing the cancer spreading to nearby lymph nodes," said Dr Ian Barron, the lead author who carried out the research at Trinity College Dublin, and is now working at Johns Hopkins in the USA. "We analyzed data from 2,796 women with stage I-III breast cancer. We found that those women prescribed aspirin in the years immediately prior to their breast cancer diagnosis were statistically significantly less likely to present with a lymph node-positive breast cancer than non-users. The association was strongest among women prescribed aspirin regularly and women prescribed higher aspirin doses. We now need to establish how and why this is the case." The findings are consistent with two other major studies. The first is an analysis of cardiovascular trials where pre-diagnostic aspirin use was associated with a statistically significant reduction in the risk of developing metastases and dying from cancer. The second is an observation from in vivo breast cancer models, which suggest a possible mechanism by which aspirin may reduce the risk of cancer spreading to other parts of the body.

Novel Approach Promises Major Treatment Advance for Neurofibromatosis-1 Patients

An enzyme therapy may prevent skeletal abnormalities associated with the genetic disorder neurofibromatosis type-1, Vanderbilt investigators have discovered. The researchers demonstrated in a mouse model of the disorder that the enzyme asfotase-alpha improves bone growth, mineralization, and strength. The findings, reported online on July 6, 2014 in Nature Medicine, “suggest that we can make bone stronger and better by injecting this drug, and possibly prevent fractures in patients with neurofibromatosis,” said Florent Elefteriou, Ph.D., director of the Vanderbilt Center for Bone Biology. While he is excited about the results, Dr. Elefteriou emphasized the challenge of moving from mouse to human studies. “It’s very difficult to set up a clinical trial in patients with a rare disease; it will have to be an international effort to pool these patients,” he said. Neurofibromatosis type-1 (NF1) is caused by mutations in the gene for neurofibromin, a protein that regulates cellular signaling pathways. The disorder causes nervous system tumors and skeletal pathologies including scoliosis, bone fragility, fracture, and pseudoarthrosis (non-union of the bone following fracture). Fractures are treated surgically to stabilize the bone and promote healing. Some families opt for amputation, to spare their children the pain of repeated surgeries, Dr. Elefteriou said. “We wondered if there might be a way to prevent the fractures from happening in the first place,” he said. It was difficult to even propose non-surgical preventive treatments, however, because it was unclear how mutations in neurofibromin cause skeletal pathologies. To investigate the molecular pathology of NF1, Dr. Elefteriou and his colleagues, including first author Jean de la Croix Ndong, Ph.D., have studied a mouse model of the disorder.