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Exosome Diagnostics Achieves ISO 13485 Certification Its USA and Germany Facilities; Company Growing into IVD Manufacturer Due to Demand for Its Instrument Platform & Companion Diagnostic Tests

On August 3, 2017, Exosome Diagnostics, Inc., a leader in the liquid biopsy market, announced that it has received ISO 13485 certification for both its USA and Germany facilities. This achievement paves the way for the company to be an In Vitro Diagnostic (IVD) medical device design and manufacturing organization. Combined with the company’s CLIA-certified Waltham, Massachusetts laboratory and ISO 15189-accredited Munich laboratory, the IVD-certified locations will serve as an integral part of the company’s strategy for the instrument platform, companion diagnostics, and diagnostics to better the lives of patients worldwide. The British Standards Institution (BSI) has certified Exosome Diagnostics under ISO 13485:2003 under CMDCAS for the following scope: “Design, development, manufacture, distribution, installation, and service of In Vitro Diagnostic (IVD) medical devices including opto-electromechanical instruments, sample collection kits, reagents, and disposables.” As defined by the International Organization for Standardization, ISO 13485 is a standard that specifies requirements for a quality management system (QMS) where an organization needs to demonstrate its ability to provide medical devices (IVDs) and related services that consistently meet customer needs and applicable regulatory requirements. “This ISO 13485 certification is a testament to the compliance initiatives undertaken by Exosome Dx to design and manufacture IVDs. Working closely with the notified body and appropriate regulatory agencies, Exosome Dx adheres to the strictest standards to provide the highest quality of products to clinicians,” stated Raaj Venkatesan, Head of Regulatory Affairs at Exosome Diagnostics.

“The Biology of Color”—New Study Explores Advances and Challenges in Field of Animal Coloration

Scientists are on a threshold of a new era of color science due largely to an explosion of technologies, but key questions remain for the field, according to a study published in the August 4, 2017 issue of Science by an international team of researchers led by Dr. Tim Caro of the University of California (UC), Davis. While studies have long used color as a factor for understanding evolution, only recently have visual physiologists, sensory and behavioral ecologists, evolutionary biologists, and anthropologists come together to study how color is produced and perceived by animals and its function and patterns of evolution. With this wide-ranging synthesis in Science, entitled "The Biology of Color," such a multidisciplinary group provides a roadmap of advances in the field of animal coloration, as well as citing remaining challenges. "In the past 20 years, the field of animal coloration research has been propelled forward very rapidly by technological advances," said corresponding author Dr. Caro, a professor in the UC Davis Department of Wildlife, Fish and Conservation Biology. "These include digital imaging, innovative laboratory and field studies, and large-scale comparative analyses, each of which is allowing completely new questions to be asked." Coloration is a complicated biological trait. Animals use it for camouflage, to send warning signals, attract mates, send social signals, regulate their body temperature, and thwart pests, among other uses. Dr. Caro's own research has helped clarify long-held mysteries about animal coloration. This includes why zebras have black and white stripes (to avoid biting flies) (https://www.ucdavis.edu/news/wildlife-biologist-earns-his-zebra-stripes-...) and why pandas are black and white (to provide camouflage in both snow and dark forests, because they need to eat year-round).

Germline Gene Correction for Inherited Genetic Disease Demonstrated in Human Embryos

Scientists have demonstrated an effective way of using a gene-editing tool to correct a disease-causing gene mutation in human embryos and stop it from passing to future generations. The new technique uses the gene-editing tool CRISPR to target a mutation in nuclear DNA that causes hypertrophic cardiomyopathy, a common genetic heart disease that can cause sudden cardiac death and heart failure. The research, published online on August 2, 2017 in Nature, demonstrates a new method of repairing a disease-causing mutation and preventing it from being inherited by succeeding generations. The article is titled “Correction of a Gene Mutation in Human Embryos.” This is the first time that scientists have successfully tested the method on donated clinical-quality human eggs. “Every generation on would carry this repair because we’ve removed the disease-causing gene variant from that family’s lineage,” said senior author Shoukhrat Mitalipov, PhD, who directs the Center for Embryonic Cell and Gene Therapy at Oregon Health and Sciences University (OHSU) in Portland, Oregon. “By using this technique, it’s possible to reduce the burden of this heritable disease on the family and eventually the human population.” The study provides new insight into a technique that could apply to thousands of inherited genetic disorders affecting millions of people worldwide. The gene-editing technique described in this study, done in concert with in vitro fertilization, could provide a new avenue for people with known heritable disease-causing genetic mutations to eliminate the risk of passing the disease to their children. It could also increase the success of IVF by increasing the number of healthy embryos.

Mysterious Children’s Neurological Disease Traced to Single Base Error in One Gene; Deep Sequencing Is Key to Discovery of Mutation Affecting Ribosomal RNA Metabolism

In a new study published on August 3, 2017 in The American Journal of Human Genetics, a multinational team of researchers describes, for the first time, the biological basis of a severe neurological disorder in children. The extremely rare disorder is characterized by developmental regression and neurodegeneration. At first, the children lead normal lives and seem identical to their age-matched peers. However, beginning at around 3 to 6 years of age, the children present with neurological deterioration, gradually losing motor, cognitive, and speech functions. Although the condition progresses slowly, most patients are completely dependent on their caretakers by 15-20 years of age. Researchers from the Hadassah Medical Center and the Hebrew University of Jerusalem’s Faculty of Medicine, working with colleagues from the Pennsylvania State University College of Medicine and a multinational research team, have now identified and studied seven children — from Canada, France, Israel, Russia, and the United States — who suffer from the disorder. The researchers found in all patients the same spontaneously occurring, non-inherited genetic change in a gene (named “UBTF”) responsible for ribosomal RNA formation. Because of this small change, the patients’ cells are flooded with ribosomal RNA and are poisoned by it. (Ribosomes are responsible for the translation and production of cell proteins; themselves, they are made up of ribosomal proteins and of ribosomal RNA in a precise ratio). The researchers found an identical error in the same gene in all the patients tested, representing a difference of one letter among the roughly 3 billion letters that make up human DNA.

Autism May Reflect Excitation-Inhibition Imbalance in Brain, Stanford Study Finds

A study by Stanford University investigators suggests that key features of autism reflect an imbalance in signaling from excitatory and inhibitory neurons in a portion of the forebrain, and that reversing the imbalance could alleviate some of its hallmark symptoms. In a series of experiments conducted on a mouse model of the disorder, the scientists showed that reducing the ratio of excitatory to inhibitory signaling countered hyperactivity and deficits in social ability, two classic symptoms of autism in humans. The study was published in the August 2, 2017 issue of Science Translational Medicine. Dr. Karl Deisseroth, Professor of Bioengineering and of Psychiatry and Behavioral Sciences, is the study's senior author. The lead author is former graduate student Aslihan Selimbeyoglu, PhD. The article is titled “Modulation of Prefrontal Cortex Excitation/Inhibition Balance Rescues Social Behavior In CNTNAP2-Deficient Mice.” In 2011, Dr. Deisseroth's group published a study in Nature showing that autism-like behavioral deficits could be induced in ordinary mice by elevating the ratio of excitatory to inhibitory neuronal firing patterns in the mice's medial prefrontal cortex. The new study shows that decreasing that ratio restores normal behavior patterns in a strain of lab mice bioengineered to mimic human autism. These mice carry a mutation equivalent to a corresponding mutation in humans that is associated with autism spectrum disorder. For reasons that are not understood, the incidence of autism spectrum disorder has increased steadily in recent years, said Dr. Deisseroth, a practicing psychiatrist. Approximately 1 in 80 American children may be diagnosed with the disorder, which is characterized by repetitive behaviors and difficulty with social interaction.

Gladstone Study Reveals How to Reprogram Cells in Our Immune System; Discovery Could Improve Treatments for Autoimmune Diseases and Cancer

When the immune system is imbalanced, either due to overly-active cells or cells that suppress its function, it causes a wide range of diseases, from psoriasis to cancer. By manipulating the function of certain immune cells, called T cells, researchers could help restore the system's balance and create new treatments to target these diseases. Scientists at the Gladstone Institutes in San Francisco revealed, for the first time, a method to reprogram specific T cells. More precisely, they discovered how to turn pro-inflammatory cells that boost the immune system into anti-inflammatory cells that suppress it, and vice versa. The researchers studied two types of cells called effector T cells, which activate the immune system to defend our body against different pathogens, and regulatory T cells, which help control the immune system and prevent it from attacking healthy parts of its environment. "Our findings could have a significant impact on the treatment of autoimmune diseases, as well as on stem cell and immuno-oncology therapies," said Gladstone Senior Investigator Sheng Ding, PhD, who is also a Professor of Pharmaceutical Chemistry at the University of California, San Francisco. By drawing on their expertise in drug discovery, Dr. Ding's team identified a small-molecule drug that can successfully reprogram effector T cells into regulatory T cells. Their study, published online on August 2, 2017 in Nature, describes, in detail, a metabolic mechanism that helps convert one cell type into another. The article is titled “Metabolic Control of TH17 and Induced Treg Cell Balance By An Epigenetic Mechanism.” This new approach to reprogram T cells could have several medical applications. For instance, in autoimmune disease, effector T cells are overly activated and cause damage to body.

Serum Exosomal miR-125b Is a Novel Prognostic Marker For Hepatocellular Carcinoma

Hepatocellular carcinoma (HCC) is the sixth most common cancer worldwide with high mortality. Circulating miRNA has been demonstrated as a novel noninvasive biomarker for many tumors. A new study by collaborators in China sought to investigate the potential of circulating miR-125b as a prognostic marker of HCC. In the work, exosomes were extracted from serum samples collected from two independent cohorts: cohort 1: HCC (n=30), chronic hepatitis B (CHB, n=30), liver cirrhosis (LC, n=30); cohort 2: HCC (n=128). The researchers found that miR-125b levels were remarkably increased in exosomes compared to those in serum from patients with CHB, LC, and HCC (P<0.01, respectively). However, miR-125b levels in exosomes and the serum from HCC patients were inferior to that of CHB (P<0.01 and P=0.06) and LC patients (P<0.01 for all). Additionally, miR-125b levels in exosomes were associated with tumor number (P=0.02), encapsulation (P<0.01), and TNM stage (P<0.01). In TMN, T describes the size of the original tumor and whether it has invaded nearby tissue; N describes nearby (regional) lymph nodes that are involved; and M describes distant metastasis. Kaplan–Meier analysis indicated that HCC patients with lower exosomal miR-125b levels showed reduced time to recurrence (TTR) (P<0.01) and overall survival (OS) (P<0.01). Furthermore, multivariate analysis revealed that miR-125b level in exosomes, but not in serum, was an independent predictive factor for TTR (P<0.001) and OS (P=0.011). Exosomal miR-125b levels predicted the recurrence and survival of HCC patients with an area under the ROC curve of 0.739 (83.0% sensitivity and 67.9% specificity) and 0.702 (82.5% sensitivity and 53.4% specificity). In conclusion, the researchers believe that exosomal miR-125b could serve as a promising prognostic marker for HCC.

Scientists Uncover Secrets of Potent DNA Toxin

One of the most potent of known toxins acts by joining the two strands of the DNA double helix together in a unique fashion which foils the standard repair mechanisms cells use to protect their DNA. A team of Vanderbilt University researchers has worked out the molecular details that explain how this bacterial toxin -- yatakemycin (YTM) -- prevents DNA replication. The team’s results, described in a paper published online on July 24, 2017 in Nature Chemical Biology, explain YTM's extraordinary toxicity and could be used to fine-tune the compound's impressive antimicrobial and antifungal properties. The article is titled “Toxicity and Repair of DNA Adducts Produced by the Natural Product Yatakemycin.” YTM is produced by some members of the Streptomyces family of soil bacteria to kill competing strains of bacteria. It belongs to a class of bacterial compounds that are currently being tested for cancer chemotherapy because their toxicity is extremely effective against tumor cells. "In the past, we have thought about DNA repair in terms of protecting DNA against different kinds of chemical insults," said Professor of Biological Sciences Brandt Eichman. "Now, toxins like YTM are forcing us to consider their role as part of the ongoing chemical warfare that exists among bacteria, which can have important side effects on human health." Cells have developed several basic types of DNA repair, including base excision repair (BER) and nucleotide excision repair (NER). BER generally fixes small lesions and NER removes large, bulky lesions. A number of DNA toxins create bulky lesions that destabilize the double helix. However, some of the most toxic lesions bond to both strands of DNA, thereby preventing the cell's elaborate replication machinery from separating the DNA strands so they can be copied.

House Spider & Venomous Scorpion Share Common Ancestor; Genome Duplication Revealed by Genome Sequencing

In collaboration with scientists from the UK, Europe, Japan, and the United States, researchers at the Human Genome Sequencing Center at Baylor College of Medicine in Houston, Texas have discovered a whole genome duplication during the evolution of spiders and scorpions. The study was published online on July 31, 2017 in BMC Biology. The open-access article is titled “The House Spider Genome Reveals an Ancient Whole-Genome Duplication During Arachnid Evolution.” Researchers have long been studying spiders and scorpions for both applied reasons, such as studying venom components for pharmaceuticals and silks for materials science, and for basic questions such as the reasons for the evolution and to understand the development and ecological success of this diverse group of carnivorous organisms. As part of a pilot project for the i5K, a project to study the genomes of 5,000 arthropod species, the Human Genome Sequencing Center analyzed the genome of the house spider Parasteatoda tepidariorum - a model species studied in laboratories - and the Arizona bark scorpion Centruroides sculpturatus, - the most venomous scorpion in North America. Analysis of these genomes revealed that spiders and scorpions evolved from a shared ancestor more than 400 million years ago, which made new copies of all of the genes in its genome, a process called whole genome duplication. Such an event is one of the largest evolutionary changes that can happen to a genome and is relatively rare during animal evolution. Dr. Stephen Richards, Associate Professor in the Human Genome Sequencing Center, who led the genome sequencing at Baylor, said, "It is tremendously exciting to see rapid progress in our molecular understanding of a species that we coexist with on planet earth.

History of Gum Disease Increases Cancer Risk in Older Women; New Study Is First to Report Association Between Periodontal Disease and Gallbladder Cancer Risk In Women or Men

Postmenopausal women who have a history of gum disease also have a higher risk of cancer, according to a new study of more than 65,000 women. The study, led by researchers at the University at Buffalo (UB) in New York, is the first national study of its kind involving U.S. women, and the first to focus specifically on older women. It's also the first study to find an association between periodontal disease and gallbladder cancer risk in women or men. The findings were published on August 1, 2017 in Cancer Epidemiology, Biomarkers & Prevention. "This study is the first national study focused on women, particularly older women," said Dr. Jean Wactawski-Wende, the study's senior author. "Our study was sufficiently large and detailed enough to examine not just overall risk of cancer among older women with periodontal disease, but also to provide useful information on a number of cancer-specific sites," added Dr. Wactawski-Wende, Dean of UB's School of Public Health and Health Professions and a Professor of Epidemiology and Environmental Health. The study included 65,869 postmenopausal women enrolled in the Women's Health Initiative, an ongoing national prospective study designed to investigate factors affecting disease and death risk in older American women. The average age of the participants was 68, and most were non-Hispanic white women. As part of a follow-up health questionnaire, participants were asked "Has a dentist or dental hygienist ever told you that you had periodontal or gum disease?" Women who reported a history of gum disease had a 14 percent increased risk of overall cancer. Of the 7,149 cancers that occurred in the study participants, the majority -- or 2,416 -- were breast cancer.

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