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Archive - Mar 6, 2017

In Infants at High Risk of Autism, MRIs Showing Increased Cerebrospinal Fluid (CSF) Predict Future Autism with Nearly 70 Percent Accuracy

A national research network led by the University of North Carolina (UNC) School of Medicine's Joseph Piven, M.D., found that many toddlers diagnosed with autism at two years of age had a substantially greater amount of extra-axial cerebrospinal fluid (CSF) at 6 and 12 months of age, before diagnosis is possible. They also found that the more CSF at six months - as measured through MRIs - the more severe the autism symptoms were at two years of age. "The CSF is easy to see on standard MRIs and points to a potential biomarker of autism before symptoms appear years later," said Dr. Piven, co-senior author of the study, the Thomas E. Castelloe Distinguished Professor of Psychiatry, and Director of the Carolina Institute for Developmental Disabilities (CIDD). "We also think this finding provides a potential therapeutic target for a subset of people with autism." The findings, published online on March 6, 2016 in Biological Psychiatry, point to faulty CSF flow as one of the possible causes of autism for a large subset of people. The article is titled “Increased Extra-axial Cerebrospinal Fluid in High-Risk Infants who Later Develop Autism.” "We know that CSF is very important for brain health, and our data suggest that in this large subset of kids, the fluid is not flowing properly," said Mark Shen, Ph.D., CIDD postdoctoral fellow and first author of the study. "We don't expect there's a single mechanism that explains the cause of the condition for every child. But we think improper CSF flow could be one important mechanism." Until the last decade, the scientific and medical communities viewed CSF as merely a protective layer of fluid between the brain and skull, not necessarily important for proper brain development and behavioral health.

Anti-Inflammatory Drug Anakinra Does Not Seem to Improve Fatigue Severity in Women with Chronic Fatigue Syndrome (CFS)

The anti-inflammatory biologic drug anakinra (interleukin-1 receptor antagonist) does not reduce fatigue severity in women with chronic fatigue syndrome (CFS), according to findings of a randomized, placebo-controlled trial, the results of which were published online on March 7, 2017 in Annals of Internal Medicine. The article is titled “Cytokine Inhibition in Patients with Chronic Fatigue Syndrome: A Randomized Trial.” CFS is characterized by severe, persistent, and disabling fatigue. In order to fulfill the Centers for Disease Control and Prevention (CDC) criteria for CFS, patients have to report at least four of eight accompanying symptoms in addition to fatigue (headache, persistent muscle pain, increased malaise [extreme exhaustion and sickness] following physical activity or mental exertion, problems with sleep, difficulties with memory and concentration, joint pain [without redness or swelling], tender lymph nodes in the neck or armpit, sore throat). Interleukin-1 (IL-1), a pro-inflammatory cytokine, has been associated with CFS in some studies. There is extensive experience with blocking IL-1 in a variety of diseases with the IL-1 receptor antagonist anakinra. Several studies in inflammatory and non-inflammatory illnesses have assessed the effect of IL-1 inhibition on fatigue severity, and most have found positive effects of this intervention. Researchers from the Radboud University Medical Centre in the Netherlands conducted a randomized, placebo-controlled trial to evaluate the effects of anakinra injections versus placebo on fatigue severity in patients with CFS. Because CFS typically affects women, the researchers included only female patients to investigate a homogeneous group.

Stream of Surprises from Atlantic Cod Genome

Researchers at the University of Oslo (UiO) in Norway keep discovering surprises in the Atlantic cod genome. The most recent study has revealed an unusual amount of short and identical DNA sequences, which might give cod an evolutionary advantage. The report was published online on January 18, 2017 in BMC Genomics in an open-access article titled “An Improved Genome Assembly Uncovers Prolific Tandem Repeats in Atlantic Cod.” Close to ten years ago, researchers from the Norwegian Institute for Water Research (NIVA) caught "Calvin the Cod" and hauled him out of the cold Arctic waters during an oceanographic expedition to the Barents Sea and the northern coast of Norway and the Lofoten archipelago. From Lofoten, Calvin’s journey took him to NIVA’s research station close to Norway’s capital Oslo. The story could have ended there, but Calvin’s destiny took a sudden twist when researchers from the University of Oslo found him swimming in a tank, killed him with a blow to the head, and took samples from his body home to their big freezer at the Department of Biosciences. An ordinary cod would have been eaten after being placed in the freezer, but Calvin the Cod instead started a new career. Calvin was in fact a healthy and characteristic representative of the population of skrei, which is the Norwegian term for cod that migrate between feeding grounds in the Barents Sea and spawning areas along the Norwegian coast. Thus, Calvin was chosen for the honorable task of donating his body parts and genes to science. In 2008, researchers at the University of Oslo initiated a unique project: they wanted to map the genome of a fish of great economic importance, namely Atlantic cod. This project has later become a huge success, and the cod genome researchers have delivered a stream of surprises, based on their studies of Calvin’s genome.

Johns Hopkins to Host Expert Panel on Challenges Surrounding Future of Immunotherapy & Precision Medicine on March 8 in Washington, DC; First Event in Precision Medicine Series

Johns Hopkins inHealth (, an initiative of Johns Hopkins aimed at moving the field of individualized health forward, will kick off a brand-new event series called the “On the Road to Precision Medicine Health Care Leader Series.” The series will address some of the challenges and obstacles faced in the field of precision medicine. The inaugural event taking place March 8, 2017 at the National Press Club in Washington, DC, will focus on the future of immunotherapy. Leading experts will gather to discuss topics such as cost, communication, research, and health care delivery “Immunotherapy: Precision Medicine in Action.” An expert panel will provide insight about the obstacles immunotherapy is facing today. The panelists will include Roy Baynes, M.D., Ph.D., Senior Vice President, Clinical Development and Chief Medical Officer, Merck Research Laboratories; Glenn Dranoff, M.D., Global Head of Exploratory Immuno-Oncology, Novartis; William Nelson, M.D., Ph.D., Director, Johns Hopkins Kimmel Cancer Center, Elizabeth Jaffee, M.D., Associate Director, Johns Hopkins Bloomberg~Kimmel Institute for Cancer Immunotherapy Deputy Director, Johns Hopkins Kimmel Cancer Center; and Margaret Anderson, Executive Director, FasterCures ( The event will be held on Wednesday, March 8, 2017, 9–10:30 a.m. EST, at the National Press Club, 529 14th St. NW, 13th Floor, Fourth Estate Room, Washington, DC 20045.

[Media alert]

New Species of Shadow-Loving Fungus Gnat Named After Founder of Symphonic Metal Band Nightwish

Tuomas Holopainen (photo), the multi-talented musician and founder of the symphonic metal band Nightwish, is also a full-blooded nature person. This gave conservation biologist Jukka Salmela, Ph.D., of Metsähallitus Parks & Wildlife Finland an idea for the name of a new species he found in Finland. Discovered in eastern Lapland during an insect survey, the fungus gnat was given the scientific name Sciophila holopaineni after Tuomas. The new species was described online in the open-access Biodiversity Data Journal on March 6, 2017. The article is titled “New and Poorly Known Palaearctic Fungus Gnats (Diptera, Sciaroidea).” "I am very, very touched. This is the highest honor a nature nerd like me can receive," Holopainen replied after Dr. Salmela, who collected and described the fungus gnat, asked him for permission to name the species after him. The idea for the name came to Salmela while he was thinking about the habitat and appearance of the species. Then, he recalled Tuomas Holopainen's interest in the natural sciences. So far, the new species of fungus gnat has only been known from two locations: the Törmäoja Natura Area in Savukoski, eastern Lapland, and a meadow close to the White Sea, Russian Karelia. The dark and beautiful gnat thrives in shadowy environments. In Törmäoja, it was caught in a river gulch next to the river source, while hiding under the shelter of the forest. Salmela proposes “tuomaanvarjokainen” as the common Finnish name, inspired by the latest Nightwish album. After all, the themes of the album, “Endless Forms Most Beautiful,” are evolution and the diversity of nature. Fungus gnats are flies that feed on dead wood or fungi. Some of the larvae are predaceous. At current count, there are almost 800 species in Finland and about 1,000 in the Nordic countries.

DNA Patterns Can Reveal How Glucose Metabolism Drives Cancer, Study Finds

A UCLA-led study of DNA patterns in tumor cells suggests that the abundance of aberrant genetic signatures common in more aggressive cancers is not random but reflects selective forces in tumor evolution. The findings also demonstrate that these changes drive glucose metabolism in cells, which can lead to accelerated cancer growth. Less aggressive cancers are known to have an intact genome — the complete set of genes in a cell — while the genome of more aggressive cancers tends to have a great deal of abnormalities. Modern research has focused largely on individual cancer genes, specifically oncogenes and tumor-suppressor genes, as the primary targets for DNA mutations and copy number alternations. Mutation or amplification in oncogenes can turn healthy cells into tumor cells. When tumor-suppressor genes are not working properly cells can grow out of control. However, scientists continue to observe many recurrent copy number alteration patterns in tumors that cannot be fully explained by these canonical cancer genes. It has long been known that a fundamental difference between healthy cells and tumor-forming cells is reprogrammed cellular metabolism. An altered metabolism benefits a transformed cell in many ways, particularly in the ability to convert glucose into energy. This process, known as glycolysis, can fuel tumor growth the most-aggressive cancers. In the five-year study, Thomas Graeber, Ph.D., UCLA Professor of Molecular and Medical Pharmacology, and his colleagues used a cross-cancer analysis of copy number alterations data from human tumors, cancer cell lines and mouse models of cancer.