In the most comprehensive assessment of its type, UNSW Australia-led research has found that in just four years, the HPV vaccine has resulted in a dramatic drop in genital warts in young Australians from a range of backgrounds, a result that could herald further good news for cervical cancer rates in future. The research, which was done in collaboration with the University of Sydney, is based on national hospital admission rates and shows a similar result in the female indigenous population, which has historically had significantly higher rates of cervical cancer. Genital warts and cervical cancer are both caused by HPV. The work was published online on August 12, 2014 in the Journal of Infectious Diseases. In the four years after the national program for school-aged girls was rolled out in 2007, there was a 90% drop in genital warts for girls aged between 12 and 17, and a 73% decrease for women between 18 and 26 years. The vaccine appeared to have an indirect protective effect among young men between the ages of 18 and 26, with a 38% drop in genital warts even prior to boys being vaccinated at school. "This is a fantastic outcome," says the senior author of the paper, Associate Professor Karen Canfell, from UNSW's Lowy Cancer Research Centre. "This is a condition which can be distressing and embarrassing and most often occurs when people start to become sexually active." The vaccine used in the National HPV Vaccination Program in Australia, Gardasil, provides protection against four strains of HPV. HPV 16 and 18 are implicated in several cancers, particularly cervical cancer. Two other strains, HPV 6 and 11 are associated with 90% of genital warts.
Colonization of methicillin-resistant Staphylococcus aureus (MRSA) allows people in the community to unknowingly harbor and spread this life-threatening bacteria. The inside of the front of the nose is where this bacteria is most predominant, but new research shows nearly all colonized individuals have this bacteria living in other body sites. The study was published in Infection Control and Hospital Epidemiology, the journal of the Society for Healthcare Epidemiology of America. "While people colonized with MRSA may not be sick, the bacteria can become aggressive and lead to infection in the person or others," said Kyle Popovich, M.D., M.S., lead author of the study. Because of the risk of transmission, hospitals have developed infection control and prevention efforts that identify individuals with nasal MRSA colonization. These patients may be placed in isolation or decolonized of MRSA by treating and removing the bacteria from the patient's nose and skin. These strategies have been used to prevent MRSA infections for the patient and to decrease risk of spread of MRSA to other patients. Several states also mandate these MRSA surveillance programs. Researchers collected surveillance swab specimens for nose and other body sites from patients at Stroger Hospital of Cook County within 72 hours of admission from March 2011-April 2012. After analyzing the samples, researchers observed that, following the nose, the rectal and groin areas were frequent sites of colonization of community-associated MRSA. The bacteria were found in these body sites more often in men than in women. "Our findings show that MRSA colonization is not limited to the nose. This may have important implications MRSA surveillance programs nationwide," said Dr. Popovich.
Spider silk is light and delicate, while incredibly resilient and tear-resistant. Understanding the structure and way of construction of these threads is a challenge taken up by a research team of Kiel University. The scientists examined five different spider species regarding the adhesion and tensile strength of a particular silk they use to fix the main thread to a surface. As shown in their new study published online on July 16, 2014 in the international Journal of the Royal Society Interface, the scientists found out that the substrate has a particularly significant impact on the silk’s adhesion. The research group led by Professor Stanislav Gorb (Institute of Zoology, Kiel University) has attended to the functional analysis of animal surfaces. Why do a gecko’s feet adhere to a wall? Why does a snake’s skin not fray out while the snake is moving forward? The group’s most recent study object is spider silk: spiders use the so-called safety thread to prevent them from falling, to lower themselves and to build the web’s framework. The threads are fixed to the surface and other threads by means of so-called attachment discs generated by rotating motions of the silk glands and applied in the form of a special lattice pattern. The scientists of Dr. Gorb’s research team investigated how attachment discs adhere to various surfaces. “To this end, we placed the spiders on glass, Teflon, and the leaf of a sycamore maple, and they produced attachment discs on each surface. Subsequently, we performed tensile tests to measure the strength necessary to detach the discs from the substrate,” says the author of the current study, Jonas Wolff.
A new study published online on August 12, 2014 in The American Journal of Pathology identifies a novel gene that controls nerve conduction velocity. Investigators report that even minor reductions in conduction velocity may aggravate disease in multiple sclerosis (MS) patients and in mice bred for the MS-like condition experimental autoimmune encephalomyelitis (EAE). A strong tool for investigating the pathophysiology of a complex disease is the identification of underlying genetic controls. Multiple genes have been implicated as contributing to the risk of developing MS. Unlike studies that have focused on genetic regulators of inflammation, autoimmunity, demyelination, and neurodegeneration in MS, this study focused on nerve conduction velocity. Investigators found that polymorphisms of the inositol polyphosphate-4-phosphatase, type II (Inpp4b) gene affect the speed of nerve conduction in both mice with EAE and humans with MS. "Impairment of nerve conduction is a common feature in neurodegenerative and neuroinflammatory diseases such as MS. Measurement of evoked potentials (whether visual, motor, or sensory) is widely used for diagnosis and recently also as a prognostic marker for MS," says lead investigator Saleh M. Ibrahim, M.D., Ph.D., of the Department of Dermatology, Venereology, and Allergology of the University of Lubeck (Germany). Using several genomic approaches, the investigators narrowed their search to the genetic region controlling the enzyme inositol-polyphosphate-4-phosphatase II (INPP4B), the product of which helps to regulate the phosphatidyl inositol signaling pathway. Enzymes in this family are involved in cellular functions such as cell growth, proliferation, differentiation, motility, survival, and intracellular communication.
Researchers at the Children’s Medical Center Research Institute at University of Texas (UT) Southwestern (CRI) have identified a gene that contributes to the development of several childhood cancers, in a study conducted with mice designed to model the human cancers. If the findings prove to be applicable to humans, the research could lead to new strategies for targeting certain childhood cancers at a molecular level. The study was published online on August 11, 2014 in Cancer Cell. “We and others have found that Lin28b (see image of cells stained with anti-Lin28b antibody)– a gene that is normally turned on in fetal but not adult tissues – is expressed in several childhood cancers, including neuroblastoma, Wilms’ tumor, and hepatoblastoma, a type of cancer that accounts for nearly 80 percent of all liver tumors in children,” said Dr. Hao Zhu, a principal investigator at CRI, and Assistant Professor of Pediatrics and Internal Medicine at UT Southwestern Medical Center. “In our study, we found that overproduction of Lin28b specifically causes hepatoblastoma, while blocking Lin28b impairs the cancer’s growth. This opens up the possibility that pediatric liver cancer patients could one day be treated without resorting to chemotherapy.” Lin28b is an attractive therapeutic target in cancer because it is ordinarily only expressed in embryos, so blocking it in children should specifically hinder cancer growth without introducing many side effects. Each year in the United States, 700 children are newly diagnosed with neuroblastoma, 500 with Wilms’ tumor, and 100 with hepatoblastoma. At Children’s Medical Center in Dallas, more than 100 children have been treated for those three types of cancers over the last two years.
Bee, snake, or scorpion venom could form the basis of a new generation of cancer-fighting drugs, scientists will report here in San Francisco today at the National Meeting of the American Chemical Society (ACS), the world's largest scientific society. They scientists have devised a method for targeting venom proteins specifically to malignant cells while sparing healthy ones, which reduces or eliminates side effects that the toxins would otherwise cause. The report was part of the 248th National Meeting of the American Chemical Society (ACS), the world's largest scientific society. The meeting, attended by thousands of scientists, features nearly 12,000 reports on new advances in science and other topics. It is being held here through Thursday. A brand-new video on the research is available at http://www.youtube.com/watch?v=GRsUi5UrH7k&feature=youtu.be. "We have safely used venom toxins in tiny nanometer-sized particles to treat breast cancer and melanoma cells in the laboratory," says Dipanjan Pan, Ph.D., who led the study. "These particles, which are camouflaged from the immune system, take the toxin directly to the cancer cells, sparing normal tissue." Venom from snakes, bees, and scorpions contains proteins and peptides which, when separated from the other components and tested individually, can attach to cancer cell membranes. That activity could potentially block the growth and spread of the disease, other researchers have reported. Dr. Pan and his team say that some of substances found in any of these venoms could be effective anti-tumor agents. But just injecting venoms into a patient would have side effects. Among these could be damage to heart muscle or nerve cells, unwanted clotting or, alternately, bleeding under the skin. So Dr.
Designing structures and devices that protect the body from shock and vibrations during high-velocity impacts is a universal challenge. Scientists and engineers focusing on this challenge might make advances by studying the unique morphology of the woodpecker, whose body functions as an excellent anti-shock structure. The woodpecker's brain can withstand repeated collisions and deceleration of 1200 g during rapid pecking. This anti-shock feature relates to the woodpecker's unique morphology and ability to absorb impact energy. Using computed tomography and the construction of high-precision three-dimensional models of the woodpecker, Chinese scientists explain its anti-shock biomechanical structure in terms of energy distribution and conversion. Their findings, presented in a new study titled "Energy conversion in the woodpecker on successive pecking and its role in anti-shock protection of the brain" and published in the Beijing-based journal SCIENCE CHINA Technological Sciences, could provide guidance in the design of anti-shock devices and structures for humans. To build a sophisticated 3-D model of the woodpecker, scientist Dr. Wu Chengwei and colleagues at the State Key Lab of Structural Analysis for Industrial Equipment, part of the Department of Engineering Mechanics at the Dalian University of Technology in northeastern China, scanned the structure of the woodpecker and replicated it in remarkable detail. "CT scanning technology can be used to obtain the images of internal structures of objects … which is widely used in the medical field and expanded to mechanical modeling of biological tissue," they explain in the study.
The protein mTOR (see image of mTOR activating mutations) is a central controller of growth and metabolism. Deregulation of mTOR signaling increases the risk of developing metabolic diseases such as diabetes, obesity, and cancer. Online on July 31, 2014 in PNAS, researchers from the Biozentrum of the University of Basel describe how aberrant mTOR signaling in the liver not only affects hepatic metabolism, but also whole body physiology. The protein mTOR regulates cell growth and metabolism and thus plays a key role in the development of human disorders. In the cell, this regulatory protein is found in two structurally and functionally distinct protein complexes called mTORC1 and mTORC2. In a recent study, the research group of Professor Michael Hall from the Biozentrum of the University of Basel has shed light on the role of hepatic mTORC1 in whole body physiology and the relevance for human liver cancers. In mammals, the liver is a key organ that controls whole body physiology in response to nutrients. Dr. Hall’s team investigated the role of the nutrient sensor mTORC1 in this process. The researchers were able to show that activation of mTORC1 in the liver of mice reduces not only hepatic lipid metabolism but also locomotor activity and body temperature. Upon investigating the underlying molecular mechanism, they observed that mTORC1 hyperactivation enhances the level of the stress hormone FGF21 by depletion of the amino acid glutamine. Treatment of animals with glutamine reduced the level of FGF21 and thus prevented the physiological impairments. Human cancers often exhibit aberrant mTORC1 signaling and glutamine addiction. “We were excited to see that in human liver tumors mTORC1 signaling correlates with FGF21 expression,” comments cell biologist Dr. Marion Cornu, the first author of the study.
Researchers have discovered a previously unknown cardiac molecule that could provide a key to treating, and preventing, heart failure. The newly discovered molecule provides the heart with a tool to block a protein that orchestrates genetic disruptions when the heart is subjected to stress, such as high blood pressure. When the research team, led by Ching-Pin Chang, M.D., Ph.D., associate professor of medicine at the Indiana University School of Medicine, restored levels of the newly discovered molecule in mice experiencing heart failure, the progression to heart failure was stopped. The research was published in the online edition of the journal Nature. The newly discovered molecule is known as a long non-coding RNA. RNA's usual role is to carry instructions -- the code -- from the DNA in a cell's nucleus to the machinery in the cell that produces proteins necessary for cell activities. In recent years, scientists have discovered several types of RNA that are not involved in protein coding but act on their own. The role in the heart of long non-coding RNA has been unknown. But the researchers determined that the newly discovered non-coding RNA, which they named Myheart -- for myosin heavy-chain-associated RNA transcript -- is responsible for controlling a protein called BRG1 (image) (pronounced "berg-1"). In earlier research published in Nature in 2010, Dr. Chang and his colleagues discovered that BRG1 plays a crucial role in the development of the heart in the fetus. But as the heart grows and needs to mature into its adult form, BRG1 is no longer needed, so very little of it is produced. That is, until the adult heart is subjected to significant stress such as high blood pressure or damage from a heart attack. Dr.
Scientists have discovered a new form of dystrophin, a protein critical to normal muscle function, and identified the genetic mechanism responsible for its production. Studies of the new protein isoform, published online on August 10, 2014 in Nature Medicine and led by a team in The Research Institute at Nationwide Children's Hospital, suggest it may offer a novel therapeutic approach for some patients with Duchenne muscular dystrophy, a debilitating neuromuscular condition that usually leaves patients unable to walk on their own by age 12. Duchenne muscular dystrophy, or DMD, is caused by mutations in the gene that encodes dystrophin, which plays a role in stabilizing the membrane of muscle fibers. Without sufficient quantities of the protein, muscle fibers are particularly susceptible to injury during contraction. Over time, the muscle degenerates and muscle fibers are slowly replaced by fat and scar tissue. Many different types of mutations can lead to DMD, some of which block dystrophin production altogether and others that result in a protein that doesn't function normally. In 2009, a team led by Kevin Flanigan, M.D., a principal investigator in the Center for Gene Therapy at Nationwide Children's, published two studies describing patients whose genetic mutation was located in a exon 1, at the beginning of the gene. This mutation should have made natural production of functioning dystrophin impossible, resulting in severe disease. However, the patients had only minimal symptoms and relatives carrying the same mutations were identified who were walking well into their 70s. Muscle biopsies revealed that, despite the genetic mutations, the patients were producing significant amounts of a slightly smaller yet functioning dystrophin. In the 2009 studies, Dr.