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Archive - Aug 2013

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August 9th

New Treatment for Brittle Bone Disease Found

A new treatment for children with brittle bone disease has been developed by scientists at the University of Sheffield and Sheffield Children’s Hospital. The study of the new treatment for children with the fragile bone disease osteogenesis imperfecta was published online on August 6, 2013 in The Lancet. This is the first study to clearly demonstrate that the use of the medicine risedronate can not only reduce the risk of fracture in children with brittle bones but also have rapid action - the curves for fracture risk begin to diverge after only six weeks of treatment. Dr. Nick Bishop, Professor of Pediatric Bone Disease at the University of Sheffield, said: “We wanted to show that the use of risedronate could significantly impact on children's lives by reducing fracture rates - and it did. The fact that this medicine can be given by mouth at home (other similar medicines are given by a drip in hospital) makes it family-friendly.” The study, funded by the Alliance for Better Bone Health, trialled children with osteogenesis imperfecta aged 4-15 years and showed that oral risedronate reduced the risk of first and recurrent clinical fractures and that the drug was generally well tolerated. For more information about osteogenesis imperfecta, visit the Brittle Bone Society (http://www.brittlebone.org/). [Press release] [The Lancet abstract]

Genetics of Planktonic Fossils May Shed New Light on Evolutionary Processes

An evolutionary ecologist at the University of Southampton in the UK, is using 'grains of sand' to understand more about the process of evolution. Dr. Thomas Ezard is using the fossils of microscopic aquatic creatures called planktonic foraminifera, often less than a millimeter in size, which can be found in all of the world's oceans. The remains of their shells now resemble grains of sand to the naked eye and date back hundreds of millions of years. A new paper by Dr. Ezard, published online on August 9, 2013 in an open-access article in the journal Methods in Ecology & Evolution, opens the debate on the best way to understand how new species come into existence (speciation). The debate concerns whether fossil records such as those of the planktonic foraminifera, contain useful evidence of speciation over and above the molecular study of evolution. Molecular evolution traditionally uses evidence from species that are alive today to determine what their ancestors may have looked like, whereas this new research promotes the importance of using fossil records in conjunction with the molecular models. Dr. Ezard, from Biological Sciences and the Institute for Life Sciences at Southampton, says: "Because planktonic foraminifera have been around for many millions of years and rocks containing groups of their species can be dated precisely, we can use their fossils to see evidence of how species evolve over time. We can also see how differences between individual members of species develop and, in theory, how a new species comes into existence. The controversial hypothesis we test is that the processes leading to a new species coming into existence provoke a short, sharp burst of rapid genetic change.

Successful Treatment of Triple Negative Breast Cancer by Modulating OGF-OGFr Axis

Researchers at The Pennsylvania State University College of Medicine, led by Dr. Ian S. Zagon, have discovered that a novel biological pathway, the OGF-OGFr (opioid growth factor-opioid growth factor receptor) axis, can be modulated in human triple-negative breast cancer cells to inhibit cancer proliferation. According to BreastCancer.org, 1 in 8 women in the U.S. will develop invasive breast cancer and more than 39,000 deaths occur annually. Approximately 15 to 20% of all breast cancers are designated as triple-negative meaning that the cancer cells lack estrogen and progesterone receptors, and do not overexpress human epidermal growth factor receptor (HER-2), thereby limiting responsiveness to approved therapy. In the June 2013 issue of Experimental Biology and Medicine, Dr. Zagon and colleagues demonstrate that exposure of human breast cancer cell lines to OGF in vitro repressed growth within 24 hours in a receptor-mediated and reversible manner. Treatment with low dosages of the opioid antagonist naltrexone (LDN) provoked a compensatory elevation in endogenous opioids (i.e., OGF) and receptors that interact for 18-20 hours daily following receptor blockade to elicit a robust inhibition of cell proliferation. Because OGF is an endogenous neuropeptide, there are minimal or no side effects. The mechanism of action for OGF is upregulation of the p21 cyclin-dependent inhibitory kinase pathway that delays passage through the cell cycle. OGF also confers some level of protection against paclitaxel treatment, a standard breast cancer therapy. A dosage of 10(-8) M paclitaxel given alone caused marked apoptosis, but resulted in 60% less cell death when given in the presence of OGF. In patients, paclitaxel often is accompanied by side effects that reduce compliance.

Whole-Genome Sequencing Reveals Mysteries of the Endangered Chinese Alligator

In a study published online on August 6, 2013 in an open-access article in Cell Research, Chinese scientists from Zhejiang University and BGI have completed the genome sequencing and analysis of the endangered Chinese alligator (Alligator sinensis). This is the first published crocodilian genome, providing a good explanation of how terrestrial-style reptiles adapt to aquatic environments and temperature-dependent sex determination (TSD). The Chinese alligator is a member of the alligator family that lives in China. It is critically endangered with a population of ~100 wild and ~10,000 captive individuals in Zhejiang and Anhui Provinces. Great efforts have been put into uncovering the mysteries of this species because of its unique features that allow the animals to be be adapted for living in both water and land habitats. In this study, researchers collected a Chinese alligator sample from Changxing Yinjiabian Chinese Alligator Nature Reserve (Zhejiang Province, China) and sequenced its genome using a whole-genome shotgun strategy. The genomic data yielded a draft sequence of Chinese alligator with the size of 2.3 Gb, and a total of 22,200 genes were predicted. The genomic data provides strong evidence from the DNA level to illustrate why the Chinese alligator can hold its breath under water for long periods of time, such as the duplication of the bicarbonate-binding hemoglobin gene, positively selected energy metabolism, and others. Researchers further identified the genetic signatures of the powerful sensory system and immune system of the Chinese alligator. All the results presented evidence for co-evolution of multiple systems specific to the back-to-the water transition. Chinese alligator exhibits TSD, and does not possess sex chromosomes. The absence of sex chromosomes is another interesting feature.

August 8th

Group of Six MicroRNAs Can Trigger Lymphomas

A small group of immune-regulating molecules, when overproduced even moderately, can trigger the blood cancers known as lymphomas, according to a new study led by scientists from The Scripps Research Institute (TSRI). The six “microRNA” molecules were already known to be overproduced in lymphomas and in many other human cancers, but no one had demonstrated that they can be the prime cause of such cancers—until now. The new study also identified the major biological pathways through which these microRNAs ignite and maintain cancerous growth. “We were able to show how this microRNA cluster can be the main driver of cancer, and so we now can start to think about therapies to combat its effects,” said TSRI Assistant Professor Changchun Xiao. Dr. Xiao was the senior investigator for the study, which was published online on August 6, 2013 in the EMBO Journal, a publication of the European Molecular Biology Organization. Discovered only in the 1990s, microRNAs are short molecules that work within virtually all animal and plant cells. Typically each one functions as a “dimmer switch” for one or more genes; it binds to the transcripts of those genes and effectively keeps them from being translated into proteins. In this way, microRNAs can regulate a wide variety of cellular processes. The focus of the new study was a cluster of six microRNAs known as miR-17~92, encoded by a single gene on chromosome 13. Studies of miR-17~92, including one from Dr. Xiao’s lab earlier this year, have shown that it controls various immune-related and developmental processes, depending on the type of cell in which it is expressed.

August 6th

BioQuick Online News Wins Fourth Straight Publication Excellence Award

BioQuick Online News (http://www.bioquicknews.com) has just been awarded an APEX 2013 Award for Publishing Excellence in the category of electronic publications. BioQuick also won prestigious APEX Publishing Excellence Awards in 2012, 2011, and 2010. BioQuick presently features over 1,200 online articles on major life science advances in the last four years and articles of interest are readily accessible by means of a powerful search engine. BioQuick now has readers in over 160 countries and includes a Japanese language edition. To find out more information about BioQuick and to pursue advertising and sponsorship possibilities in this high-quality, far-reaching life science publication, please contact editor & publisher Mike O’Neill (M.A. in Immunology & Microbioloy from Duke) at logophile2000@yahoo.com. To learn more about the highly competititive APEX Publishing Awards, please visit the awards web site at http://www.apexawards.com. One indicator of the overall quality of the competition is the high-quality organizations numbering among the winners.

August 1st

Trace Substance in Caramelized Sugar Improves Muscle Regeneration in Fly and Mousel Models of Muscular Dystrophy

A trace substance in caramelized sugar, when purified and given in appropriate doses, improves muscle regeneration in a mouse model of Duchenne muscular dystrophy. The findings were published online on August 1, 2013 in an open-access article in the journal Skeletal Muscle. Dr. Morayma Reyes, professor of pathology and laboratory medicine, and Dr. Hannele Ruohola-Baker, professor of biochemistry and associate director of the Institute for Stem Cell and Regenerative Medicine, headed the University of Washington (UW) team that made the discovery. The first authors of the paper were Dr. Nicholas Ieronimakis, UW Department of Pathology; and Dr. Mario Pantoja, UW Department of Biochemistry. The authors explained that the mice in their study, like boys with the gender-linked inherited disorder muscular dystrophy, are missing the gene that produces dystrophin, a muscle-repair protein. Neither the mice nor the affected boys can replace enough of their routinely lost muscle cells. In people, muscle weakness begins when the boys are toddlers, and progresses until, as teens, they can no longer walk unaided. During early adulthood, their heart and respiratory muscles weaken. Even with ventilators to assist breathing, death usually ensues before age 30. No cure or satisfactory treatment is available. Prednisone drugs relieve some symptoms, but at the cost of severe side effects. The disabling, then lethal, nature of the rare disease in young men presses scientists to search for better therapeutic agents. Dr. Reyes and Dr. Ruohola-Baker are seeking ways to suppress the disorder's characteristic functional and structural muscle defects. Dr. Ruohola-Baker's lab originally identified the sphingosine 1-phosphate (S1P) pathway as a critical player in ameliorating muscular dystrophy in flies.

August 1st

Scientists Identify Staph-Killing Compound That May Be Effective in Osteomyelitis

Osteomyelitis, a debilitating bone infection most frequently caused by Staphylococcus aureus ("staph") bacteria, is particularly challenging to treat. Now, Vanderbilt microbiologist Eric Skaar, Ph.D., M.P.H., and colleagues have identified a staph-killing compound that may be an effective treatment for osteomyelitis, and they have developed a new mouse model that will be useful for testing this compound and for generating additional therapeutic strategies. James Cassat, M.D., Ph.D., a fellow in Pediatric Infectious Diseases who is interested in improving treatments for children with bone infections, led the mouse model studies. Working with colleagues in the Vanderbilt Center for Bone Biology and the Vanderbilt University Institute of Imaging Science, Dr. Cassat developed micro-computed tomography (micro-CT) imaging technologies to visualize a surgically introduced bone infection in progress. "The micro-CT gives excellent-resolution images of the damage that's being done to the bone," said Dr. Skaar, the Ernest W. Goodpasture Professor of Pathology. "We found that staph is not only destroying bone, but it's also promoting new bone growth. Staph is causing profound changes in bone remodeling." Dr. Cassat also established methods for recovering -- and counting -- bacteria from the infected bone. "We're not aware of any other bone infection models where you can pull the bacteria out of a bone and count them in a highly reproducible manner," Dr. Skaar said. "From a therapeutic development standpoint, we think this model is going to allow investigators to test new compounds for efficacy against bone infections caused by staph or any other bacteria that cause osteomyelitis." Several pharmaceutical companies have already approached Dr.

Japanese Scientists ID Inflammatory On/Off Switch for Allergic Asthma and COPD

Japanese researchers have made a new step toward understanding—and learning how to stop—runaway inflammation for both chronic obstructive pulmonary disorder (COPD) and allergic asthma. In a new report appearing in the August 2013 issue of The FASEB Journal the scientists show that two receptors of an inflammatory molecule, called "leukotriene B4," play opposing roles in turning inflammation on and off for allergic asthma and COPD. The first receptor, called "BLT1," promotes inflammation, while the second receptor, called "BLT2," has a potential to weaken inflammation during an allergic reaction. This discovery also is important because until now, BLT2 was believed to increase inflammatory reaction. "Leukotriene B4 levels are elevated in the airways of the patients with asthma and COPD, and the opposite role of BLT1 and BLT2 in allergic inflammation implies that drug development should target BLT1 and BLT2 differently," said Hiromasa Inoue, M.D., study author from the Department of Pulmonary Medicine at the Graduate School of Medical and Dental Sciences at Kagoshima University in Kagoshima, Japan. "We hope that better anti-asthma drugs or anti-COPD drugs will be produced in the future to treat millions of patients who suffer from severe asthma and COPD." To make this discovery, scientists compared the allergic reactions in BLT2-gene deleted mice to those in normal mice. Then an allergic asthma reaction was provoked by inhalation of allergens. BLT2-gene deleted mice showed more inflammatory cells in the lung compared to normal mice. Without the BLT2 gene, lung allergic inflammation was stronger than that of normal mice. The production of interleukin-13, an important mediator of allergic inflammation from T lymphocytes, was increased in the group without the BLT2 gene.

Fetal Stress May Cause Epigenetic Changes That Pose Long-Term Risk Factors for Chronic Disease

If you think stress is killing you, you may be right, but what you don't know is that stress might have harmed your health even before you were born. In a new report appearing in the August 2013 issue of The FASEB Journal, Harvard researchers find that epigenetic disruptions, which are associated with chronic disease later in life, are already common at birth. Possibly, these aberrations result from stressors in the intrauterine environment (e.g., maternal smoking, maternal diet, or high levels of endocrine-disrupting chemicals). This finding supports the belief that seeds of disease are sown before birth, increasing the importance of optimal prenatal care. "This study may help us understand whether epigenetic mechanisms contribute to chronic disease susceptibility already prior to birth," said Karin Michels, Sc.D., Ph.D., study author from Harvard Medical School. "We are currently exploring which stressors during prenatal life may contribute to these epigenetic disruptions." To make this discovery, Dr. Michels and colleagues examined the expression pattern of imprinted genes important for growth and development. Researchers analyzed the parental expression pattern in the cord blood and placenta of more than 100 infants and followed up this analysis with methylation and expression studies. The results lent credence to the emerging theme that susceptibility to disease may indeed originate in utero. Additionally, this research showed that a high degree of disruption occurred during the imprinting of a gene called IGF2, which was expressed from both alleles in the cord blood of 22 percent of study subjects. Loss of imprinting of IGF2 has been associated with several cancers, including Wilms tumor, colorectal and breast cancer, and childhood disorders such as Beckwith-Wiedemann syndrome.