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Archive - 2014

Fibromyalgia and the Role of Brain Connectivity in Pain Inhibition

The cause of fibromyalgia, a chronic pain syndrome, is not known. However, the results of a new study that compares brain activity in individuals with and without fibromyalgia indicate that decreased connectivity between pain-related and sensorimotor brain areas could contribute to deficient pain regulation in fibromyalgia, according to an article published in Brain Connectivity, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The article is available free on the Brain Connectivitywebsite at until November 1, 2014. The new study by Dr. Pär Flodin and coauthors from the Karolinska Institutet (Stockholm, Sweden) builds on previous findings in fibromyalgia that showed abnormal neuronal activity in the brain associated with poor pain inhibition. In the current study, "Fibromyalgia Is Associated with Decreased Connectivity between Pain- and Sensorimotor Brain Areas," the researchers report a pattern of "functional decoupling" between pain-related areas of the brain that process pain signals and other areas of the brain, such as those that control sensorimotor activity in fibromyalgia patients compared to healthy patients, in the absence of any external pain stimulus. As a result, normal pain perception may be impaired. "Fibromyalgia is an understudied condition with an unknown cause that can only be diagnosed by its symptoms," says Christopher Pawela, Ph.D., Co-Editor-in-Chief of Brain Connectivity and Assistant Professor, Medical College of Wisconsin. He was not involved in the current study. "This study by Flodin et al.

First-Ever Field Evidence of Controversial “Group Selection” Found in Social Spiders

Along rivers in Tennessee and Georgia, scientists have been studying brownish-orange spiders, called Anelosimus studiosusm (image), that make cobwebby nests “anywhere from the size of a golf ball to the size of a Volkswagen Beetle,” researcher Dr. Jonathan Pruitt says. The individual spiders are only the size of a pencil eraser, but they form organized groups that can catch prey ranging from fruit flies to small vertebrates. “We have found carcasses of rats and birds inside their colonies,” Dr. Pruitt says. Unlike most spiders, which are solitary, these social spiders work together in groups. Now new research shows that they evolve together in groups, too. Mention the term “group selection” among some groups of evolutionary biologists and you won’t be invited back to the party. But Dr. Pruitt, at the University of Pittsburgh, and Dr. Charles Goodnight, at the University of Vermont, have been studying generations of these Anelosimus spiders — and have gathered the first-ever experimental evidence that group selection can fundamentally shape collective traits in wild populations. Their results were published online on October 1, 2014 in Nature. “Biologists have never shown an adaptation in nature which is clearly attributable to group selection,” Dr. Goodnight said. “Our paper is that demonstration.” In his 1859 masterpiece, “On the Origin of Species,” Charles Darwin puzzled over how ants could — generation after generation — produce workers that would serve the colony — but were sterile. Evolution by natural selection has often been understood to work at the level of the organism: the traits of an individual determine whether it will survive and reproduce. How could these sterile ants persist in nature, he wondered, if they didn’t reproduce?

Long Non-Coding RNAs Fine-Tune the Immune System

Regulation of the human immune system's response to infection involves an elaborate network of complex signaling pathways that turn on and off multiple genes. The emerging importance of long noncoding RNAs and their ability to promote, fine-tune, and restrain the body's inflammatory response by regulating gene expression is described in a review article published online on September 24, 2014 in the Journal of Interferon & Cytokine Research (JICR), a peer-reviewed publication from Mary Ann Liebert, Inc., publishers. In the article "Transcription of Inflammatory Genes; Long Non-Coding RNA and Beyond,” Drs. Susan Carpenter and Katherine Fitzgerald, University of Massachusetts Medical School, Worcester, Massachusetts, and University of California, San Francisco, Califonia, respectively, provide a detailed overview of the multi-layered gene regulation systems that are activated when the immune system recognizes a pathogen or other external danger signal. The growing understanding of the role that long noncoding RNAs play in regulating this complex circuitry could lead to their use as drug targets for developing selective antimicrobial therapeutics that do not cause damaging inflammation. "This is a cutting-edge review from authors who are conducting pioneering research on the role of long non-coding RNAs in innate immune signaling," says Journal of Interferon & Cytokine Research Co-Editor-in-Chief Ganes C. Sen, Ph.D., Chairman, Department of Molecular Genetics, Cleveland Clinic Foundation, Ohio. [Press release] [Journal of Interferon & Cytokine Research]

New Absorber Will Lead to Better Biosensors

Biological sensors, or biosensors, are like technological canaries in the coal mine. By converting a biological response into an optical or electrical signal, they can alert us to dangers in our external and internal environments. They can sense toxic chemicals and particles in the air and enzymes, molecules, and antibodies in the body that could indicate diabetes, cancer, and other diseases. An optical biosensor works by absorbing a specific bandwidth of light and shifting the spectrum when it senses minor changes in the environment. The narrower the band of absorbed light is, the more sensitive the biosensor. “Currently, plasmonic absorbers used in biosensors have a resonant bandwidth of 50 nanometers,” said Dr. Koray Aydin, assistant professor of electrical engineering and computer science in the McCormick School of Engineering at Northwestern University in Chicago. “It is significantly challenging to design absorbers with narrower bandwidths.” Dr. Aydin and his team have created a new nanostructure that absorbs a very narrow spectrum of light—having a bandwidth of just 12 nanometers. This ultranarrow band absorber can be used for a variety of applications, including better biosensors. “We believe that our unique narrowband absorber design will enhance the sensitivity of biosensors,” Dr. Aydin said. “It’s been a challenge to sense very small particles or very low concentrations of a substance.” This research was described in the paper “Ultranarrow band absorbers based on surface lattice resonances in nanostructured metal surfaces,” published in the August 26, 2014 issue of ACS Nano. Typical absorber designs use two metal sheets with a non-metallic insulating material in between. By using nanofabrication techniques in the lab, Dr.

Breakthrough in Understanding of T-Cell Selection for Antigen Reactivity

Research by University of California Irvine (UC Irvine) immunologists reveals new information about how our immune system functions, shedding light on a vital process that determines how the body’s ability to fight infection develops. In the online version of Nature Immunology published on September 28, 2014, neurology professor Dr. Michael Demetriou, postdoctoral scholar Dr. Raymond Zhou, and other Institute for Immunology colleagues describe a critical mechanism underlying how T-cells are created, selected, and released into the bloodstream. A T- cell (image) is a type of blood cell called a lymphocyte that protects the body from infection. T-cell precursors called thymocytes are created in the bone marrow and migrate to the thymus – a walnut-sized organ at the base of the neck – where they are transformed into T-cells. However, very few thymocytes become fully functional T-cells, and in the current study, the Demetriou team gained important new insights into why. As they are transformed into T-cells, thymocytes grow receptors that react to an antigen (any substance provoking an immune response) that’s bound to a small molecule called MHC major histocompatibility complex). If this reaction is too strong or too weak, the thymocyte does not mature into a T-cell. Dr. Demetriou and the others found that the delicate balance determining the proper reactive ability is controlled by glycosylation, a process in which a sugar attaches to a target protein to give the protein stability and form. They saw that changes in the addition of sugars to receptors – including the blocking of glycosylation – during T-cell development profoundly influenced how thymocytes reacted to the MHC-bound antigens and whether they became mature T-cells.

Blades of Grass Inspire Major Nanotech Advance in Organic Solar Cells

Using a bio-mimicking analog of one of nature's most efficient light-harvesting structures, blades of grass, an international research team led by Dr. Alejandro Briseno, of the University of Massachusetts (U Mass) Amherst, has taken a major step in developing long-sought polymer architecture to boost power-conversion efficiency of light to electricity for use in electronic devices. Dr. Briseno, with colleagues and graduate students at U Mass Amherst and others at Stanford University and Dresden University of Technology, Germany, reported online on September 16, 2014 in Nano Letters that by using single-crystalline organic nanopillars, or "nanograss," they found a way to get around dead ends, or discontinuous pathways, that pose a serious drawback when using blended systems known as bulk heterojunction donor-acceptor, or positive-negative (p-n), junctions for harvesting energy in organic solar cells. Dr. Briseno's research group is one of very few in the world to design and grow organic single-crystal p-n junctions. He says, "This work is a major advancement in the field of organic solar cells because we have developed what the field considers the 'Holy Grail' architecture for harvesting light and converting it to electricity." The breakthrough in morphology control should have widespread use in solar cells, batteries, and vertical transistors, he adds. Dr. Briseno explains, "For decades scientists and engineers have placed great effort in trying to control the morphology of p-n junction interfaces in organic solar cells.

September 30th

Rare Disease Gene Identified; May Lead to Progress on Devasting Genetic Disease and Also Cancer

The discovery of a gene mutation that causes a rare premature aging disease could lead to the development of drugs that block the rapid, unstoppable cell division that makes cancer so deadly. Scientists at the University of Michigan (U-M) and the U-M Health System recently discovered a protein mutation that causes the devastating Hoyeraal-Hreidarsson syndrome, a specific form of dyskeratosis congenital (DC), in which precious hematopoietic stem cells can't regenerate and make new blood. People with DC age prematurely and are prone to cancer and bone marrow failure. But the study findings reach far beyond the roughly one in 1 million known DC patients, and could ultimately lead to developing new drugs that prevent cancer from spreading, said Dr. Jayakrishnan Nandakumar, assistant professor in the U-M Department of Molecular, Cellular, and Developmental Biology. The DC-causing mutation occurs in a protein called TPP1 (image). The mutation inhibits TPP1's ability to bind the enzyme telomerase to the ends of chromosomes, which ultimately results in reduced hematopoietic stem cell division. While telomerase is underproduced in DC patients, the opposite is true for cells in cancer patients. "Telomerase overproduction in cancer cells helps them divide uncontrollably, which is a hallmark of all cancers," Dr. Nandakumar said. "Inhibiting telomerase will be an effective way to kill cancer cells." The findings could lead to the development of gene therapies to repair the mutation and start cell division in DC patients, or drugs to inhibit telomerase and cell division in cancer patients. Both would amount to huge treatment breakthroughs for DC and cancer patients, Dr. Nandakumar said.

Transplant Drug Rapamycin Could Boost Power of Immune-Based Brain Tumor Treatments

Every day, organ transplant patients around the world take a drug called rapamycin (image) to keep their immune systems from rejecting their new kidneys and hearts. New research suggests that the same drug could help brain tumor patients by boosting the effect of new immune-based therapies. In experiments in animals, researchers from the University of Michigan (U-M) Medical School showed that adding rapamycin to an immunotherapy approach strengthened the immune response against brain tumor cells. What's more, the drug also increased the immune system's "memory" cells so that they could attack the tumor if it ever reared its head again. The mice and rats in the study that received rapamycin lived longer than those that didn't. Now, the U-M team plans to add rapamycin to clinical gene therapy and immunotherapy trials to improve the treatment of brain tumors. They currently have a trial under way at the U-M Health System which tests a two-part gene therapy approach in patients with brain tumors called gliomas in an effort to get the immune system to attack the tumor. In future clinical trials, adding rapamycin could increase the therapeutic response. The new findings, published online on September 25, 2014 in Molecular Cancer Therapeutics, show that combining rapamycin with a gene therapy approach enhanced the animals' ability to summon immune cells called CD8+ T cells to kill tumor cells directly. Due to this cytotoxic effect, the tumors shrank and the animals lived longer. But the addition of rapamycin to immunotherapy, even for a short while, also allowed the rodents to develop tumor-specific memory CD8+ T cells that remember the specific "signature" of the glioma tumor cells and attacked them swiftly when a tumor was introduced into the brain again.

MaxBin Software: Automated Binning of Individual Genomes from Metagenomes

Microbes – the single-celled organisms that dominate every ecosystem on Earth – have an amazing ability to feed on plant biomass and convert it into other chemical products. Tapping into this talent has the potential to revolutionize energy, medicine, environmental remediation, and many other fields. The success of this effort hinges in part on metagenomics, the emerging technology that enables researchers to read all the individual genomes of a sample microbial community at once. However, given that even a teaspoon of soil can contain billions of microbes, there is a great need to be able to cull the genomes of individual microbial species from a metagenomic sequence. Enter MaxBin, an automated software program for binning (sorting) the genomes of individual microbial species from metagenomic sequences. Developed at the U.S. Department of Energy (DOE)’s Joint BioEnergy Institute (JBEI), under the leadership of Dr. Steve Singer, who directs JBEI’s Microbial Communities Group, MaxBin facilitates the genomic analysis of uncultivated microbial populations that can hold the key to the production of new chemical materials, such as advanced biofuels or pharmaceutical drugs. “MaxBin automates the binning of assembled metagenomic scaffolds using an expectation-maximization algorithm after the assembly of metagenomic sequencing reads,” says Dr. Singer, a chemist who also holds an appointment with Berkeley Lab’s Earth Sciences Division. “Previous binning methods either required a significant amount of work by the user, or required a large number of samples for comparison. MaxBin requires only a single sample and is a push-button operation for users.” The key to the success of MaxBin is its expectation-maximization algorithm, which was developed by Dr. Yu-Wei Wu, a post-doctoral researcher in Dr.

Researchers Explain 38-Year Mystery of Heart Failure: Disordered Structure of Troponin I

In a new study published online on September 22, 2014 in PNAS, researchers at the University of Alberta's Faculty of Medicine & Dentistry in Canada have explained how the function of a key protein in the heart changes in heart failure. Heart disease is the number-one killer in the developed world. The end stage of heart disease is heart failure, in which the heart cannot pump enough blood to satisfy the body's needs. Patients become progressively short of breath as the condition worsens, and they also begin to accumulate fluid in the legs and lungs, making it even more difficult to breathe. The molecular structure of the heart muscle changes as heart failure progresses, though scientists cannot always agree on what changes are good or bad. One change that occurs is an increase in "calcium sensitivity." Calcium ions are pumped in and out of the muscle cell with each heartbeat, turning contractions on and off. When the calcium sensitivity increases, contractility increases, but at a price: the relaxation of the heart becomes slower. Both phases of cardiac function are important: impaired contraction leads to systolic heart failure, while impaired relaxation leads to diastolic heart failure. Both types of heart failure are similar in terms of overall prevalence, symptoms, and mortality. Since 1976, medical researchers have known that the heart regulates its calcium sensitivity by phosphorylating a key cardiac protein called troponin I. The troponin complex is made up of three proteins, C, I, and T, which trigger muscle contraction in response to calcium. In heart failure, the phosphate groups are removed from troponin I, but it wasn't known how this caused an increase in calcium sensitivity. Dr.