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Archive - Dec 12, 2014


Ebola Lifespan Outside the Body Unknown, Despite Many Expert Claims

The Ebola virus travels from person to person through direct contact with infected body fluids. But how long can the virus survive on glass surfaces or countertops? How long can it live in waste water when liquid wastes from a patient end up in the sewage system? In an article published December 9, 2014 in the journal Environmental Science & Technology Letters, Dr. Kyle Bibby of the University of Pittsburgh reviews the latest research to find answers to these questions. He and his co-investigators did not find many answers. "The World Health Organization has been saying you can put (human waste) in pit latrines or ordinary sanitary sewers and that the virus then dies," says Dr. Bibby, assistant professor of civil and environmental engineering in Pitt's Swanson School of Engineering. "But the literature lacks evidence that it does. They may be right, but the evidence isn't there." Dr. Bibby and colleagues from Pitt and Drexel University explain that knowing how long the deadly pathogen survives on surfaces, in water, or in liquid droplets is critical to developing effective disinfection practices to prevent the spread of the disease. Currently, the World Health Organization guidelines recommend to hospitals and health clinics that liquid wastes from patients be flushed down the toilet or disposed of in a latrine. However, Ebola research labs that use patients' liquid waste are supposed to disinfect the waste before it enters the sewage system. Dr. Bibby's team set out to determine what research can and can't tell us about these practices. The researchers scoured scientific papers for data on how long the virus can live in the environment. They found a death of published studies on the matter.

Mutations in GTPBP3 Gene Cause Severe Mitochondria-Based Disease

Diseases of dysfunctional mitochondria are relatively rare, with a prevalence of 1/2000-4000. They predominantly affect children, however adult-onset disorders are also recognized. An international collaborative effort of fifteen clinical and/or research centers from the UK, Germany, Ireland, France, Belgium, Austria Italy, Israel, and Japan led by Dr. Michal Minczuk from the MRC MBU in Cambridge and Dr. Holger Prokisch from the Institute of Human Genetics, Helmholtz Centre in Munich resulted in the discovery that mutations in the GTPBP3 (GTP-binding protein 3) gene cause defects in protein synthesis in mitochondria and are associated with a devastating disease. The patients affected by this disease have deficiency in energy production and suffer from heart and neurological disease. The research was reported in the December 4, 2014 issue of the American Journal of Human Genetics in an open-access article. Mitochondria are compartments present in every cell of the body (except red blood cells) and are responsible for generating almost all of the energy needed by the body to sustain life and to grow. In mitochondria, energy is produced by a large number of proteins, which are manufactured according to a blueprint, the cell’s DNA. Most of these proteins are encoded by DNA that is contained within the cell nucleus (nuclear DNA), however, the remaining portion is encoded within a small DNA molecule found inside mitochondria. This molecule is called mitochondrial DNA (mtDNA) or the mitochondrial genome. The mitochondrial DNA must be transcribed into RNA and the RNA translated into proteins. If the mitochondrial genome is not properly expressed, then mitochondrial proteins will not be properly made, and the cell will not be able to produce energy in a useful form.

Cause of Malaria Drug Resistance in SE Asia Identified

Growing resistance to malaria drugs in Southeast Asia is caused by a single mutated gene inside the disease-causing Plasmodium falciparum parasite, according to a study led by David Fidock, Ph.D., professor of microbiology & immunology and of medical sciences (in medicine) at Columbia University Medical Center. This finding provides public health officials around the world with a way to look for pockets of emerging resistance and potentially eliminate them before they spread. Though malaria deaths have dropped by 30 percent worldwide since the introduction of artemisinin-based combination therapies (ACTs) in the late 1990s, these gains are now threatened by the emergence of resistance to the core artemisinin component of ACTs in Southeast Asia. No alternative therapy is currently available to replace ACTs should resistance spread to other parts of the world. The current study, published online on December 11, 2014 in Science, builds on a recent report that mutations in the gene--K13--are frequently found in drug-resistant parasites in Southeast Asia. Dr. Fidock, working with scientists at the Pasteur Institutes in Paris and Cambodia, the University of Toulouse III, Sangamo Biosciences, Inc., and the National Institutes of Health (NIH), showed definitively that K13 mutations directly cause drug resistance. "The bad news about our finding is that it shows that resistance can arise through single mutations in one gene and pop up anywhere, at any time," Dr. Fidock says. "That's quite different from past instances with former first-line drugs, when complex sets of multiple mutations were required and resistance spread only as the mutated parasites spread."

Possible Way to Boost Healthy Cells During Chemotherapy

It’s well known that chemotherapy helps fight cancer. It’s also known that it wreaks havoc on normal, healthy cells. Michigan State University (MSU) scientists are closer to discovering a possible way to boost healthy cell production in cancer patients as they receive chemotherapy. By adding thymine – a natural building block found in DNA – into normal cells, they found it stimulated gene production and caused the cells to multiply. The study was published online on ecember 4, 2014 in Molecular Cell. In most cases, cancer patients who receive chemotherapy lose their fast-growing normal cells, including hair, nails, and lining of the gut,” said Dr. Sophia Lunt, a postdoctoral research associate who led the study along with Dr. Eran Andrechek, a physiology professor at MSU. “Therefore, it’s necessary to understand the differences between normal versus cancer cells if we want to improve cancer therapy, while minimizing the harsh side effects.” Thymine is made from sugar in the body and is necessary to make DNA. The research team wanted to understand how fast-growing normal cells metabolize sugar and other nutrients to stimulate growth compared to fast-growing cancer cells. They were surprised to discover that when a shared protein, found in both normal and cancer cells, was removed from the healthy ones, growth stopped. Previous studies have shown that deleting this protein, known as PKM2, from the cancer cells has no effect on cancer growth. “When we deleted the protein, we found it caused healthy cells to stop making DNA,” Dr. Andrechek said. “But when we added thymine, they began multiplying and producing DNA again.” Both researchers view this as a positive step in finding ways to boost healthy cell production, but indicate that more needs to be known on the effect thymine might have on cancer cells.

Collaboration Sheds New Light on Age-Related Macular Degeneration

Insilico Medicine along with scientists from Vision Genomics and Howard University shed light on AMD disease, introducing the opportunity for eventual diagnostic and treatment options. The scientific collaboration among Vision Genomics, Inc., Howard University, and Insilico Medicine, Inc., has revealed encouraging insight on the AMD disease using an interactome analysis approach. Resources such as publicly available gene expression data, Insilico Medicine's original algorithm OncoFinder™, and AMD Medicine™ from Vision Genomics allowed discovery of signaling pathways activated during AMD disease. "We are thrilled to collaborate with Drs. Alex Zhavoronkov and Evgeny Makarev, and their team at InSilico Medicine. Big Data analysis is part of the future of medicine, and with our technique of signaling pathway activation analysis, we will decipher the genetic network alterations that lead to age-related macular degeneration (AMD), and eventually human aging itself," said Antonei Benjamin Csoka, Ph.D., CEO of Vision Genomics, LLC, and Assistant Professor at Howard University. The research publication titled "Pathway activation profiling reveals new insights into Age-related Macular Degeneration and provides avenues for therapeutic interventions" was accepted by one of aging research's top-rated journals "Aging", detailing these findings and methodology. This study not only validates the efficacy of interactome analysis within aging, but also allows the investigation of cellular populations within AMD models. "We are happy to collaborate with Antonei Benjamin Csoka's teams at both Vision Genomics and Howard University on this exciting project.

Controversial Nitrite Hypothesis Confirmed

Understanding how nitrite can improve conditions such as hypertension, heart attack, and stroke has been the object of worldwide research studies. New research from Wake Forest University has potentially moved the science one step closer to this goal. In a paper published online on December 3, 2014 in the Journal of Biological Chemistry, senior co-author Dr. Daniel Kim-Shapiro, professor of physics at Wake Forest, and others, show that deoxygenated hemoglobin is indeed responsible for triggering the conversion of nitrite to nitric oxide, a process that affects blood flow and clotting. “We have shown that conversion of nitrite to nitric oxide by deoxygenated hemoglobin in red blood cells reduces platelet activation,” Dr. Kim-Shapiro said. “This action has implications in treatments to reduce clotting in pathological conditions including sickle cell disease and stroke.” In 2003, Dr. Kim-Shapiro collaborated with Dr. Mark Gladwin, now at the University of Pittsburgh, who led a study that showed that nitrite (which is also used to cure processed meats), is not biologically inert as had been previously thought, but can be converted to the important signaling molecule nitric oxide (NO), and thereby increase blood flow. At that time, the researchers hypothesized that the conversion of nitrite to NO was due to a reaction with deoxygenated hemoglobin in red blood cells. The main goal of the latest research, Dr. Kim-Shapiro said, was to determinehow red blood cells perform these important signaling functions that lead to increased blood flow. The researchers used several biophysical techniques to measure NO production from nitrite and red blood cells and examined the mechanism of NO production.

Biofilms Associated with Proximal Colon Cancer; Possible Diagnostic Tool

Since the first “catalog” of the normal bacterial makeup of the human body was published in 2012, numerous connections between illness and disturbances in the human microbiota have been found. This week, scientists report yet another: cancerous tumors in the ascending colon (the part nearest to the small intestine) are characterized by biofilms, which are dense clumps of bacterial cells encased in a self-produced matrix. “This is the first time that biofilms have been shown to be associated with colon cancer, to our knowledge,” says co-author Dr. Jessica Mark Welch, a scientist at the Marine Biological Laboratory (MBL) in Woods Hole, Massachusetts. The discovery, led by researchers at the Johns Hopkins Medical Institutions, draws on a novel way to “see” microbial community structure that was developed by Dr. Mark Welch and colleagues at the MBL. Called combinatorial imaging, it could potentially be used to clinically diagnose pre-cancerous and cancerous conditions in the ascending colon. In healthy people, the colon is covered in a mucus layer (mucosa) that helps keep bacteria away from the colon’s “skin,” or epithelia. Remarkably, the team found that colon cancer patients who have tumor-associated biofilms also have biofilms on tumor-free areas of the nearby mucosa. “This suggests that either the tumor allows the biofilm to form, or the biofilm is helping to cause the tumor,” says Dr. Welch. “The breaching of the mucus layer could allow bacteria to come into contact with the host epithelial cells, and that is one thing that could lead to cancer.” The team found that tumors in the descending colon (going to the rectum) do not have associated biofilms.

New Dopamine-Related Target Identified for Possible Treatment of Parkinson’s

Researchers in Montréal, Canada, led by Jacques Drouin (image), D.Sc., have uncovered a mechanism regulating dopamine levels in the brain by working on a mouse model of late-onset Parkinson’s disease. The study, conducted in collaboration with Dr. Rory A. Fisher from the Department of Pharmacology at the University of Iowa Carver College of Medicine, was published online on December 11, 2014 in the open-access journal PLOS Genetics. Using gene expression profiling, a method to measure the activity of thousands of genes, researchers investigated dopaminergic neurons in the midbrain, which are nerve cells that use dopamine to send signals to other nerve cells. These neurons are known to degenerate in Parkinson’s disease. “We identified the Rgs6 gene for its restricted expression in dopaminergic neurons,” explains Dr. Drouin, Director of the Molecular Genetics laboratory at the IRCM (Institut de Recherche Clinique de Montreal). “We had previously shown that this gene is itself controlled by a transcription factor called Pitx3, which plays an important role in the survival of these neurons. Through our study, we discovered that a defective Rgs6 gene causes the death of these neurons,” adds Dr. Drouin. “More specifically, we found that when we remove the Rgs6 gene, this relieves a brake against excessive dopaminergic signalling. As a result, excess free dopamine accumulation causes cellular stress, which, in turn, causes the neurons to die. Our work thus indicates that Rgs6 could be a new target for the development of drugs against Parkinson’s disease.”