Scientists make advance in cancer research

Jan. 3, 2014 — A protein that has been at the center of cancer drug design for the last 20 years should not be given up on according to new research from the University of East Anglia (UEA).

The most advanced version of αvβ3-integrin antagonists failed clinical trials to treat aggressive forms of brain cancer.

But research published today in the American Heart Association's journal Circulation Research shows that targeting the protein in question could still be vital in stopping the growth of tumors. Not least because the drugs targeting it cause minimal side effects compared to other drugs -- which can cause bleeding in the gut and high blood pressure.

tumors must recruit their own blood supply to grow beyond a very small size. The research team studied the cells that line blood vessels (endothelial cells) in mice, and in particular the role of a widely expressed protein called beta3-integrin.

Dr Stephen Robinson, from UEA's school of Biological Sciences, said: "This protein has been the focus of drug design over the last two decades because its expression is vastly increased in endothelial cells during blood vessel recruitment.

"The most advanced of these drugs, however, has recently failed a phase III clinical trial to treat an aggressive form of brain cancer. In line with other clinical work, patients respond to treatment for a short while but then their cancers escape the treatment.

"This research helps to explain why these very promising drugs aren't meeting with the success that was anticipated and it suggests a way forward -- how to make them work better.

"We have shown how tumors continue to grow despite treatment which should block blood vessel recruitment. They modulate how they are recruiting their blood vessels by using a different pathway from the one that is being targeted. We have identified some molecular changes in endothelial cells that occur with long-term inhibition of beta3-integrin that might help the cells escape the beta3-integrin blockade.

"Our research also shows that timing is critical when targeting the protein beta3-integrin.

"Importantly, these findings have re-established the expression of beta3-integrin as a valid clinical target when treating cancer. Efforts must now be re-focused to either develop new drugs to target beta3-integrin, or figure out how to more effectively use the drugs that already exist."

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Research proposes alternative therapy against lung cancer

Jan. 6, 2014 — Research from the National Institute of Respiratory Diseases (INER) informs that besides smoking, there are other factors associated to the development of lung cancer such as the smoke from burning lumber and coal, as well as pollutant particles.

"It has been considered that the upturn in cases of lung cancer is possibly related to this particles," explains Patricia Gorocica from the INER, who, alongside her research team, has been working in an alternative therapy to boost the immune system of patients with this disease.

The specialist adds that since several years ago is known that the immune system has all the mechanism to watch and destroy tumor cells as they develop, but sometimes this mechanisms are not effective for reasons associated to the tumor or alterations of the patients organism.

Based in this principle, research at INER is directed to regulate the immune system against tumors. The tumor that can be more easily eliminated are the ones that express specific antigens.

Patricia Gorocica, chief of the Department of Biochemical Research at INER, details that with current technology is possible to manipulate the immune response against tumors. "We are developing at the lab a system of cell activation from the patient's own blood so it can eliminate its tumors."

This is a starting research, but it could be consolidated as an alternative therapy for the patients with lung cancer. The labor is being done with the support of the institutes of Biotechnology and Chemistry of the Autonomous National University of Mexico (UNAM), hoping that others will add to the cause, since this research requires a multi-disciplinary team for succeeding.

Gorocica adds that manipulating the immune system could be a new complementary therapy to chemo and radiotherapy usually used for treating lung cancer.

The research at INER is mainly focused in patients with lung adenocarcinoma, a type of cancer that has the most alterations in its tumor cells. It usually affects people of various ages, accentuated in people over 40, but has been known to affect the 20-something population.

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May predict response to Imaging Research anti new crude tumor

Advanced image processing technology for patients with tumor responds to angiogenesis drug therapy, able to distinguish which one might be. Patient's brain tumor glioma risk, Massachusetts General Hospital (Dana Farber Cancer Institute component) of researchers report, for those whose treatment anti angiogenesis drug cediranib and rapidly of their tumors around of abnormal blood vessels that "normalize" and who cediranib did not increase blood flow of patients significantly the longer survival tumor in a blood flow increases and newly diagnosed. Displays the report in PNAS Early Edition.

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Cancer cells are controlled by epigenetic processes, new research shows

First time USC Norris Comprehensive Cancer Center (home) of Keck new research from medicine, according to epigenetics in the description of the human body a natural killer (NK) cells, kill can contain viruses and cancerous tumors can be manipulated. Opens the way to develop a National Science Academy of advanced discovery more effective cancer drugs.

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Tapping a valuable resource or invading the environment? Research examines the start of fracking in Ohio

Sep. 25, 2013 — A new study is examining methane and other components in groundwater wells, in advance of drilling for shale gas that's expected over the next several years in an Ohio region.

Amy Townsend-Small, a University of Cincinnati assistant professor of geology, will present on the study on Sept. 27, at the 10th Applied Isotope Geochemistry Conference in Budapest, Hungary.

The team of UC researchers spent a year doing periodic testing of groundwater wells in Carroll County, Ohio, a section of Ohio that sits along the shale-rich Pennsylvania-West Virginia borders. The study analyzed 25 groundwater wells at varying distances from proposed fracking sites in the rural, Appalachian, Utica Shale region of Carroll County. Because the region is so rural, the majority of the population relies on groundwater wells for their water supply.

"This is a major area for shale gas drilling in Ohio, and one reason is because shales in the area are thought to have a good amount of liquid fuel as well as natural gas," says Townsend-Small.

The researchers are currently analyzing samples from groundwater wells over a one-year period, with water samples drawn every three-to-four months.

The samples are being analyzed for concentrations of methane as well as hydrocarbons -- a carcinogenic compound -- and salt, which is pulled up in the fracking water mixture from the shales, which are actually ancient ocean sediments.

"We're examining changes over time resulting from fracking, and since this is just beginning in Ohio, we have the opportunity to make some baseline assessments," says Townsend-Small.

Hydraulic fracturing, or fracking, involves using millions of gallons of water mixed with sand and chemicals to break up organic-rich shale to release natural gas resources. Proponents say fracking promises a future in lower energy prices, cleaner energy and additional jobs amid a frail economy. Opponents raise concerns about the practice leading to increased methane gas levels (known as the greenhouse gas) and other contamination -- resulting from spillover of fracking wastewater -- of groundwater in shale-rich regions.

Townsend-Small explains that some groundwater wells naturally hold a certain level of methane due to the decomposition of organic matter. It's not toxic in drinking water, but high levels can result in explosion. The study includes measurements of stable isotopes, which can indicate whether methane is derived from natural organic matter decomposition or from fossil fuels.

Other chemicals in fracking wastewater are toxic and dangerous for drinking water. Future UC research includes measurements of some of these compounds, as fracking progresses in the region.

The U.S. Energy Information Administration reported this summer that natural gas reserve additions in 2011 ranked as the second-largest annual increase since 1977, with hydraulic fracturing adding to increased oil and gas reserves.

The Ohio Department of Natural Resources reports that 882 sites in the state of Ohio have been awarded permits for fracking. In Carroll County, 327 sites have been awarded permits and 236 have been drilled.

Funding for the UC study was supported in coordination with UC Foundation by a $20,000 grant from the Missouri-based Deer Park Foundation, a $2,500 grant from the Cincinnati-based David and Sara Weston Foundation and an $85,714 grant from the Ohio Board of Regents.

Townsend-Small and her colleagues in the UC Department of Geology were also awarded a $400,000, 3-year grant from the National Science Foundation (EAR-1229114) for an isotope ratio mass spectrometer. The instrument measures the stable isotope composition of methane, which can indicate whether it is derived from biological activity or natural gas.

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Racism Takes a Toll on Kids' Mental Health, Research Shows

SUNDAY, Sept. 22 (HealthDay News) -- Being a victim of racism may trigger poor mental health, depression and anxiety in children and teens, according to a new review.

The report, published in the October issue of the journal Social Science & Medicine, looked at 461 cases of links between racism and the health and well-being of youngsters.

"The review showed there are strong and consistent relationships between racial discrimination and a range of detrimental health outcomes such as low self-esteem, reduced resilience, increased behavior problems and lower levels of well-being," lead researcher Naomi Priest, of the University of Melbourne in Australia, said in a university news release.

Most of the racism experienced by children and teens involved discrimination by other people, rather than institutional or systemic racism, according to the findings.

The review also revealed an increased risk of poorer birth outcomes among children whose mothers experienced racism during pregnancy.

Most of the studies included in the review were conducted in the United States with participants aged 12 to 18. Of the racial/ethnic groups included in the studies, the three most common were blacks, Hispanics and Asians.

"We know that children who experience poor health and well-being are less likely to engage in education, employment and other activities that support them to lead healthy and productive lives, and to participate meaningfully in the community," Priest said.

So, she noted, the findings identify an important issue that needs to be addressed in order to improve child and teen health.

More information

CivilRights.org explains the importance of talking to children about racism and diversity.

Copyright c 2013?HealthDay. All rights reserved.

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Worm research: Right combination of sugars regulates brain development

Sep. 19, 2013 — If the development of our nervous system is disturbed, we risk developing serious neurological diseases, impairing our sensory systems, movement control or cognitive functions. This is true for all organisms with a well-developed nervous system, from man to worm. New research from BRIC, University of Copenhagen reveals how a tiny molecule called mir-79 regulates neural development in roundworms. The molecule is required for correct migration of specific nerve cells during development and malfunction causes defects in the nervous system of the worm. The research has just been published in the journal Science.

Hundreds of worms lie in a small plastic plate under the laboratory microscope. Over the last three years, the group of Associate Professor Roger Pocock has used the roundworm C. elegans to study the development of the nervous system. They have just made an important discovery.

"Our new results show that a small molecule called mir-79 is indispensable for development of the worm's nervous system. mir-79 acts by equipping special signal molecules with a transmitter, which tells the nerve cells how they should migrate during development of the worm. If we remove mir-79 with gene technology, development of the worm nervous system goes awry," says postdoc Mikael Egebjerg Pedersen, who is responsible for the experimental studies.

Mir-79 adds just the right combination of sugar

The research shows that mir-79 acts by controlling the addition of certain groups of sugars to selected signaling molecules. In the world of cells, sugar molecules act as transmitters.

When the nerve cells come into contact with the sugar-transmitters, they are informed where to locate themselves during neural development. If the researchers remove mir-79, the migration of the nerve cells is misguided causing neuronal defects in the worms.

"It has earlier been shown that signaling molecules guide nerve migration, but our research shows that mir-79 regulates nerve cell migration by controlling the correct balance of sugar-transmitters on signaling molecules. If mir-79 does not function, the worm nervous system is malformed. In the wild, such defects would be harmful for worm survival," says Roger Pocock who leads the research group behind the finding.

Worm studies reveal important clues for neuronal repair

A version of mir-79 called mir-9 is found in humans. Therefore, these results are important for understanding how our nervous system develops during fetal development. In addition, the results add to the understanding of how nerve cells may be stimulated to repair damage in our brain or spinal cord.

"Our nervous system is a tissue which is not easily repaired after damage. So, how certain molecular cues can stimulate nerve cells to migrate is an important brick in the puzzle. This will enable us to understand how nerve tissue can be regenerated after, for example, a stroke or an accident. If we can use such knowledge to mimic the signals, we may be able to stimulate nerve cells to migrate into a damaged area," says Roger Pocock.

Worms are a fantastic model to study how the nervous system develops and how nerve cells form neuronal circuits. Most of the genes that control nervous system development in the worm are also found in humans. At the same time, the reduced complexity of the worm nervous system allows researchers to investigate central biological mechanisms. With new technologies they can mark single cells or molecules, and as worms are transparent, the researchers can track the marked molecules or cells live during worm development.

The next step for the researchers is to investigate how the regulatory pathway they have revealed is regulated in cultures of human cells.

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Groundbreaking pain research

Sep. 19, 2013 — The bodies of mammals, including humans, respond to injury by releasing endogenous opioids -- compounds that mitigate acute pain. A team of researchers led by those at the University of Kentucky has uncovered groundbreaking new information about how the body responds to traumatic injury with the development of a surprisingly long-lasting opioid mechanism of natural chronic pain control. Remarkably, the body develops both physical and physiological dependence on this opioid system, just as it does to opiate narcotic drugs. The research is featured on the cover of the current issue of the prestigious journal Science.

The paper, titled Constitutive Mu-Opioid Receptor Activity Leads to Long-term Endogenous Analgesia and Dependence, was authored by a team including lead author Bradley Taylor of the University of Kentucky College of Medicine Department of Physiology. Other authors include: Gregory Corder, Suzanne Doolen and Renee Donahue of the UK Department of Physiology; Brandon Jutras of the UK College of Medicine Department of Microbiology, Immunology and Molecular Genetics; Michelle Winter and Kenneth McCarson of the University of Kansas; Ying He, Zaijie Wang and Xiaoyu Hu of the University of Illinois; Jeffrey Wieskopf and Jeffrey Mogil of McGill University; and Daniel Storm of the University of Washington.

The scientists examined opioid function at sites of pain modulation in the spinal cord. When the opioids act at opioid receptor proteins, they "put the brakes" on the transmission of pain signals to the brain. For example, opioids are released when a patient undergoes surgery, a soldier is wounded in battle, or an athlete runs a marathon. Researchers have known for a while that blocking opioid receptors can increase the intensity of acute pain -- the pain occurring immediately after injury. But up to this point, scientists had been unsure whether blocking opioids could increase chronic, long-term pain. They began their work with the idea that the opioid system is much more important than previously recognized, with an ability to indefinitely oppose chronic pain. If true, they reasoned, then blocking opioids should increase chronic pain.

To simulate human injury, the researchers produced inflammation, or skin incision, in a mouse model, then waited several weeks for signs of pain-like behaviors to subside. They then administered opioid receptor blockers, effectively halting the pain-relieving actions of the opioid system. When the opioid system (which the authors use the term MORCA, for mu opioid receptor constitutive activity) was blocked, the mice reverted to a set of behaviors associated with the experience of pain. Surprisingly, they also experienced symptoms similar to the known effects of opioid withdrawal in the drug addict: tremor, jumping and shakiness. These results were observed even up to six and a half months after pain had seemingly resolved. The long-lasting nature of the phenomenon suggests that endogenous opioid analgesia silently continues long after an injury has healed.

In other words, long after an acute injury has healed, MORCA continues to "put the brakes" on pain. When MORCAis blocked, the "accelerator" is allowed to run free, and chronic pain reappears.

Because the body appears to develop a reliance on MORCA that parallels the addiction of a synthetic opioid user, and because it is known that stress is a key factor in causing relapse in opioid addicts, it follows that stress may also be a key factor in relapse in chronic pain patients. Thus, the authors speculate that stress could interfere with endogenous MORCA analgesia, leading to the emergence of widespread, rampant chronic pain such as is observed in a range of conditions, including fibromyalgia.

This research provides some answers to how the body responds to pain, but also raises questions. To return to the "brake and accelerator" metaphor, future studies are needed to better understand the long-term consequences of simultaneously pressing the accelerator and the brake on pain. In other words, how can we either prevent the "brake pads" from wearing out, or replace them when they do?

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Health research is essential for progress towards universal health coverage

15 August 2013 | Beijing - At the launch of the "World health report 2013: Research for universal health coverage", WHO today called on countries to continue investing in local research in order to develop a system of universal health coverage tailored to each individual country’s situation. With universal health coverage, countries can help ensure that citizens obtain the health services they need without suffering financial hardship when paying for them.

Dr Margaret Chan, Director-General of WHO, describes universal coverage as “the single most powerful concept that public health has to offer.” In launching the "World health report 2013: Research for universal health coverage", Dr Chan says “universal coverage is the best way to cement the health gains made during the previous decade. It is a powerful social equalizer and the ultimate expression of fairness.”

The role of research for universal health coverage

The report shows how countries, when developing a system for universal health coverage, can use research to determine what health issues should be addressed, how a system should be structured and how to measure progress according to their specific health situation.

Universal health coverage is the single most powerful concept that public health has to offer.

Dr Margaret Chan, WHO Director-General

The report reveals that, on average, domestic investment in research in low- and middle-income countries has been growing 5% each year. This trend is most visible in emerging economies such as Brazil, China and India, all of which have embraced the concept of universal health coverage.

Case studies from many countries demonstrate the importance of local and global research for improving health, ranging from the prevention and control of specific diseases to the better functioning of health systems. The results of these studies emphasize the critical need for research to be carried out locally, where researchers can consider specific factors critical to individual countries.

“Research for universal health coverage is not a luxury; rather, it is fundamental to the discovery, development and delivery of interventions that people need to maintain good health,” the report notes.

The growth of health research

The report also shows that more health research is being published as a result of international collaboration. Scientists from low- and middle-income countries are increasingly engaged in these collaborations, although high-income countries continue to play a prominent role in most studies. China is one example: from 2000 to 2010 the global share of Chinese researchers as co-authors on published research increased from 5% to 13%. Brazil, India and other countries have also increased their participation in published research. However, although research is increasing overall, growth is uneven.

“All nations should be producers as well as consumers of research. The creativity and skill of researchers are the backbone of academic and public health programs,” says Dr Christopher Dye, Director, Office of Health Information, HIV/AIDS, Tuberculosis, Malaria and Neglected Tropical Diseases and lead author of the report. “A wide range of basic and applied research studies is essential to reach universal health coverage, but gaps between knowledge and action are being closed very slowly. We need to accelerate the process of bringing scientists and decision makers together to improve health service coverage.”

Universal health coverage requires a strong, efficient, well-run health system; a system for financing health services; access to essential medicines and technologies, and sufficient well-trained, motivated health workers.

To meet the challenges, WHO encourages international donors and national governments not only to invest in research, but also to support mechanisms for sharing information and data, to strengthen research training and institutions, and to measure progress against their own commitment to achieving universal health coverage.

For more information please contact:

Helen Yu
Communications Officer
WHO in China
Telephone: +86 10 65327191
Mobile: +86 139 1 1205167
Email: yuji@wpro.who.int

Glenn Thomas
Communications Officer
WHO, Geneva
Telephone: +41 22 791 3983
Mobile: +41 79 509 0677
E-mail: thomasg@who.int

Gregory Hartl
Coordinator
News, Social Media and Monitoring, WHO
Telephone: +41 22 7914458
Mobile: +41 79203 6715
E-mail: hartlg@who.int

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Beyond peer review: Finding a way to manage errors in research data

Sep. 17, 2013 — Traditional peer review is not enough to ensure data quality amid the recent boom in scientific research findings, according to results of a 10-year collaboration between the National Institute of Standards and Technology (NIST) and five technical journals.

While production of research data is growing about 7 percent annually, about one-third of papers submitted to participating journals contained erroneous or incomplete chemical property data, according to a report by 32 authors from NIST and the collaborating journals. Poor data can lead to mistakes in equipment selection, over-design of industrial plant components, difficulty simulating and discovering new processes, and poor regulatory decisions, the report notes.

The traditional peer-review process is under pressure to work too fast to evaluate fully all new experimental data, the NIST-journal collaboration found. The authors' solution is a set of customized software tools and procedures for validating experimental data and eliminating errors after a paper is approved by peer review, but before a journal formally accepts the paper.

The collaboration focused on thermophysical property data used in chemical process technologies such as distillation, extraction and crystallization.*? Thermophysical properties include boiling and melting points, density, viscosity, solubility and many other physical values related to temperature, including those for mixtures. The study findings also may be of broad value to scientific data publishing in general.

"The solutions we offer, while centered on the field of thermodynamics, should be applicable in principle to other areas of science and engineering," says Michael Frenkel, a co-author of the new paper and leader of NIST's Thermodynamics Research Center.

Managing thermophysical property data is particularly challenging because some 100-year-old data remain useful today for engineering purposes. Efforts to establish data-reporting standards for this field began more than 50 years ago but could not succeed until recently, with the development of specialized computer hardware and software tools.

The collaboration cites a variety of factors contributing to poor data quality. Advances in measurement science have boosted data collection, but increased automation has resulted in the loss of personnel expertise and knowledge required to run manual systems. In addition, equipment manufacturers sometimes make invalid uncertainty claims. And word processing software, with functions such as cut-and-paste and "fill down" in spreadsheets, has led to many published errors. The most common problem found in papers analyzed by the collaboration was missing or underestimated uncertainties for reported data.

After several tries, the collaboration developed a rapid, cost-effective process for identifying and eliminating errors. NIST developed a new online tool (NIST ThermoLit) that allows researchers to generate a literature report containing relevant references retrieved from a NIST database. Researchers can combine this capability with an older experiment planning system (NIST ThermoPlan) at both the conceptualization and publication stages of their work. If the submitted paper passes a journal's peer review, NIST generates a report noting any inconsistencies between the new experimental data and critically evaluated data based on past research. Data are extracted from the submitted paper and validated by NIST's expert software system for data evaluation (NIST ThermoData Engine).

The NIST-journal collaboration plans to continue its work by refining and expanding the modeling and prediction tools in the expert system software.

*The five journals are Journal of Chemical and Engineering Data, Fluid Phase Equilibria, The Journal of Chemical Thermodynamics, the International Journal of Thermophysics and Thermochimica Acta.

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Research points to promising treatment for macular degeneration

Sep. 13, 2013 — Researchers at the University of North Carolina School of Medicine have published new findings in the hunt for a better treatment for macular degeneration. In studies using mice, a class of drugs known as MDM2 inhibitors proved highly effective at regressing the abnormal blood vessels responsible for the vision loss associated with the disease.

"We believe we may have found an optimized treatment for macular degeneration," said senior study author Sai Chavala, MD, director of the Laboratory for Retinal Rehabilitation and assistant professor of Ophthalmology and Cell Biology & Physiology at the UNC School of Medicine. "Our hope is that MDM2 inhibitors would reduce the treatment burden on both patients and physicians."

The research appeared Sept. 9, 2013 in the Journal of Clinical Investigation.

As many as 11 million Americans have some form of macular degeneration, which is the most common cause of central vision loss in the western world. Those with the disease find many daily activities such as driving, reading and watching TV increasingly difficult.

Currently, the best available treatment for macular degeneration is an antibody called anti-VEGF that is injected into the eye. Patients must visit their doctor for a new injection every 4-8 weeks, adding up to significant time and cost.

"The idea is we'd like to have a long-lasting treatment so patients wouldn't have to receive as many injections," said Chavala. "That would reduce their overall risk of eye infections, and also potentially lower the economic burden of this condition by reducing treatment costs." Chavala practices at the Kittner Eye Center at UNC Health Care in Chapel Hill and New Bern.

All patients with age-related macular degeneration start out with the "dry" form of the disease, which can cause blurred vision or blind spots. In about 20 percent of patients, the disease progresses to its "wet" form, in which abnormal blood vessels form in the eye and begin to leak fluid or blood, causing vision loss.

While anti-VEGF works by targeting the growth factors that lead to leaky blood vessels, MDM2 inhibitors target the abnormal blood vessels themselves causing them to regress -- potentially leading to a lasting effect.

Chavala and his colleagues investigated the effects of MDM2 inhibitors in cell culture and in a mouse model of macular degeneration. They found that the drug abolishes the problematic blood vessels associated with wet macular degeneration by activating a protein known as p53. "p53 is a master regulator that determines if a cell lives or dies. By activating p53, we can initiate the cell death process in these abnormal blood vessels," said Chavala.

MDM2 inhibitors also have conceivable advantages over another treatment that is currently being investigated in several clinical trials: the use of low-dose radiation for wet macular degeneration. Radiation works by causing DNA damage in cells leading to an increase in p53 and cell death. MDM2 inhibitors activate p53 without causing DNA damage. Also, MDM2 inhibitors can be given by eye injection, which is advantageous over some forms of radiation treatment that require surgery to administer.

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New technology transforms research in viral biology

Sep. 11, 2013 — Researchers at The Mount Sinai Medical Center have developed an innovative system to test how a virus interacts with cells in the body -- to see, for example, what happens in lung cells when a deadly respiratory virus attacks them.

In the journal Cell Host & Microbe, investigators say such a technique will not only speed basic research into viral biology, it will also help scientists improve vaccine production, generate novel antiviral compounds, and advance the development of viruses that attack cancer cells.

"We have a powerful system in place today to investigate ways in which viruses interact with cells, which has yielded fundamental insights. But has significant limitations such as cost, difficulty of use, and the problem that the cells we have to use are not in any way physiologically relevant to the virus we want to study," said the senior investigator, Benjamin tenOever, PhD, Fishberg Professor in the Department of Medicine and Department of Microbiology at the Icahn School of Medicine at Mount Sinai.

"The new system that we developed is much less costly, can be transferrable from the study of one virus to another, and, best of all, allows us to use the real virus in the real environment it infects," Dr. tenOever said.

Both the old and new systems essentially do the same thing -- they test the effect of the virus on every one of the "host factors" in a cell. Given that genomes encode about 25,000 different genes, each of which produces a different protein or molecule, researchers test what happens to viral growth and replication when each of those 25,000 factors are silenced. "By systematically silencing every one of those host cell factors, we can theoretically pinpoint a single protein that allows a virus to grow quickly, or another one that stops viral infection," Dr. tenOever said.

The technique in use today employs small interfering RNA (siRNA) molecules to silence the expression of genes in the host cell -- a robotic arm introduces a distinctive siRNA to small populations of human or animal cells.

But the system requires cells that are easy to grow as a substitute for natural cells. Immortal cancer cells or fibroblasts (connective cells) are often used, "which are not relevant in any way to the cells that most viruses attack. In order to study viruses this way, researchers have to modify them so that they can grow in these cells. This doesn't represent an accurate disease model," Dr. tenOever said. "If you want to know how flu viruses cause disease, you really want to look in the lungs or lung tissue of mammals -- which has not been possible in this kind of screen."

To make that possible, the researchers gave viruses the capacity to make those siRNAs -- eliminating the need for robots to administer individual siRNAs to individual host cells. "We created a virus family identical in all respects, except that each member of the family carries a different siRNA," Dr. tenOever says. "So in this swarm of viral soldiers, each one has a very small trick up its sleeve -- it can silence one thing in the host cell. And because of this, we can use the cells that viruses actually infect -- such as lung cells."

The researchers modified an alphavirus -- a class of viruses that includes a microbe that produces encephalitisso that 10,000 family "members" each carried a distinct siRNA -- which acts as a barcode of sorts. Then they allowed the virus to infect mice by mimicking the natural route of infection, such as a mosquito bite, and "let nature do its work," Dr. tenOever said. "We let evolution select for those viruses whose individual capacity to eliminate one thing gives them the growth advantage to outgrow their brothers and sisters." A week after the modified virus infection, researchers were able to "see" which virus grew faster than others, and could read the barcode that indicated which gene was silenced. They could also pinpoint the viruses that quickly died in cells. Such findings not only help researchers understand how the virus operates within the cell it infects, but also reveal excellent host targets for which to design antiviral drugs.

Once the virus family is generated for study, it can be amplified, so there is no need to re-engineer the virus library again, he added.

This screening system will likely have many clinical care applications, Dr. tenOever said. "It could be used to generate cell cultures that allow enhanced vaccine production. You could improve the capacity of a therapeutic virus to get into a particular tissue, to kill tumor cells, or to chase after metastatic cancer cells," he said. "There is potentially no end to uses of this technology."

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Bad news for prey: New research shows that predators can learn to read camouflage

Sep. 10, 2013 — Camouflaged creatures can perform remarkable disappearing acts but new research shows that predators can learn to read camouflage.

The study, which used human subjects as predators searching for hidden moths in computer games, found that the subjects could learn to find some types of camouflaged prey faster than others.

The research was carried out by the University of Exeter and the University of Cambridge and is published in the journal PLOS ONE. Moths with high contrast markings -- that break up the shape of the body, like that of a zebra or giraffe -- were best at evading predation at the start of the experiment. However humans learnt to find these prey types faster than moths with low contrast markings that match the background, like that of a stick insect or leaf bug.

The study shows that the benefit of a camouflage strategy depends on both how well it prevents initial detection and also on how well it inhibits learning.

Lead author Dr Jolyon Troscianko from Biosciences at the University of Exeter said: "This is the first time that a study has focused on the learning of different camouflage types rather than how quickly camouflage prevents initial detection.

"We found considerable differences in the way that predators learn to find different types of camouflage.

"If too many animals all start to use the same camouflage strategy then predators are likely to learn to overcome that strategy more easily, so prey species should use different camouflage strategies to stay under the radar. This helps to explain why such a huge range of camouflage strategies exist in nature."

Camouflage offers a visual example of how the process of natural section works in evolution. Those prey with successful camouflage strategies evade predation, survive and reproduce giving rise to future generations of successfully camouflaged individuals. Camouflage is probably the most widespread way of preventing predation in nature and is also valuable in human military applications as well as in recreation, art and fashion.

Hunt for hidden birds in new online game

Master of disguise the African nightjar has excellent camouflage that makes it very difficult to spot. The researchers have launched an online game 'Find the nightjar' where players are challenged to search for real nightjars hidden against the background of the African bush. The results will be used to help the researchers find out about animal perception and how it differs between predator types.

Take part in the online game.

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Health research is essential for progress towards universal health coverage

15 August 2013 | Beijing - At the launch of the "World health report 2013: Research for universal health coverage", WHO today called on countries to continue investing in local research in order to develop a system of universal health coverage tailored to each individual country’s situation. With universal health coverage, countries can help ensure that citizens obtain the health services they need without suffering financial hardship when paying for them.

Dr Margaret Chan, Director-General of WHO, describes universal coverage as “the single most powerful concept that public health has to offer.” In launching the "World health report 2013: Research for universal health coverage", Dr Chan says “universal coverage is the best way to cement the health gains made during the previous decade. It is a powerful social equalizer and the ultimate expression of fairness.”

The report shows how countries, when developing a system for universal health coverage, can use research to determine what health issues should be addressed, how a system should be structured and how to measure progress according to their specific health situation.

Universal health coverage is the single most powerful concept that public health has to offer.

Dr Margaret Chan, WHO Director-General

The report reveals that, on average, domestic investment in research in low- and middle-income countries has been growing 5% each year. This trend is most visible in emerging economies such as Brazil, China and India, all of which have embraced the concept of universal health coverage.

Case studies from many countries demonstrate the importance of local and global research for improving health, ranging from the prevention and control of specific diseases to the better functioning of health systems. The results of these studies emphasize the critical need for research to be carried out locally, where researchers can consider specific factors critical to individual countries.

“Research for universal health coverage is not a luxury; rather, it is fundamental to the discovery, development and delivery of interventions that people need to maintain good health,” the report notes.

The report also shows that more health research is being published as a result of international collaboration. Scientists from low- and middle-income countries are increasingly engaged in these collaborations, although high-income countries continue to play a prominent role in most studies. China is one example: from 2000 to 2010 the global share of Chinese researchers as co-authors on published research increased from 5% to 13%. Brazil, India and other countries have also increased their participation in published research. However, although research is increasing overall, growth is uneven.

“All nations should be producers as well as consumers of research. The creativity and skill of researchers are the backbone of academic and public health programs,” says Dr Christopher Dye, Director, Office of Health Information, HIV/AIDS, Tuberculosis, Malaria and Neglected Tropical Diseases and lead author of the report. “A wide range of basic and applied research studies is essential to reach universal health coverage, but gaps between knowledge and action are being closed very slowly. We need to accelerate the process of bringing scientists and decision makers together to improve health service coverage.”

Universal health coverage requires a strong, efficient, well-run health system; a system for financing health services; access to essential medicines and technologies, and sufficient well-trained, motivated health workers.

To meet the challenges, WHO encourages international donors and national governments not only to invest in research, but also to support mechanisms for sharing information and data, to strengthen research training and institutions, and to measure progress against their own commitment to achieving universal health coverage.

Helen Yu
Communications Officer
WHO in China
Telephone: +86 10 65327191
Mobile: +86 139 1 1205167
Email: yuji@wpro.who.int

Glenn Thomas
Communications Officer
WHO, Geneva
Telephone: +41 22 791 3983
Mobile: +41 79 509 0677
E-mail: thomasg@who.int

Gregory Hartl
Coordinator
News, Social Media and Monitoring, WHO
Telephone: +41 22 7914458
Mobile: +41 79203 6715
E-mail: hartlg@who.int

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Research discovers the young woman on the value of screening mammograms.

New analysis was found to occur in young women not receive mammograms at regular intervals of the number of deaths from breast cancer. 609 Was at 29 percent among women between the breast cancer mortality rate, women of undisclosed 71 percent in mammography was shown in. Boston (Dana Farber Cancer Institute component) of the study, led by scientists at Harvard Medical School cancer published earlier at the American Cancer Society peer review journal online.

Learn to read the full text of the press release.

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Among the research institutions in NCI funding, all over the United States that current cancer specifies 68 as a Center. Based at research universities, these facilities are cancer's origin and development of intense laboratory research wide range, the scientists from NCI support many home. Cancer Center program is also focused on cross-cutting research, population Sciences, and clinical research please. Center for research results are often at the forefront of cancer research.

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Research Gets to Root of Redheads' Higher Melanoma Risk

THURSDAY, Aug. 22 (HealthDay News) -- It's well known that natural redheads are at higher odds for deadly melanoma skin cancer, and new research in mice may help explain why.

Researchers at Harvard Medical School say the genetic mutation responsible for red hair and light skin also appears to promote a well-known cancer-causing pathway.

A person's hair color and skin tone are influenced by a gene receptor called melanocortin-1 (MC1R), and a mutation in MC1R accounts for the 1 percent to 2 percent of people who are born redheads.

In experiments with mice and cell cultures, researchers found that the same MC1R mutation -- called MC1R-RHC -- triggers a specific biochemical signaling pathway when a redhead is exposed to ultraviolet radiation from the sun and other sources.

This pathway, called P13K/Akt, has been tied to breast, ovarian and lung tumors, according to the study, which was published online Aug. 22 in the journal Molecular Cell.

"[The findings] provide a possible molecular mechanism as to why red-haired individuals harboring [these] mutations are much more susceptible to UV-induced skin damage than individuals with darker skin, resulting in a 10- to 100-fold higher frequency of melanoma," study co-senior author Wenyi Wei, an investigator at Beth Israel Deaconess Medical Center and an associate professor of pathology at Harvard, said in a medical center news release.

The researchers also said their findings are a starting point for future studies. For example, people who carry the MC1R mutation might be identified as being at higher skin cancer risk, or drugs that target the P13K/Akt pathway might help treat certain melanomas.

Melanoma is among the rarest of skin cancers, but it also is the most deadly, accounting for 75 percent of skin cancer deaths, the researchers said.

Researchers note that research conducted in animals often does not have the same results in humans.

More information

The U.S. National Cancer Institute has more about melanoma and other skin cancers.

SOURCE: Beth Israel Deaconess Medical Center, news release, Aug. 22, 2013

Copyright c 2013 HealthDay. All rights reserved.

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Alzheimer's research fraud case set for trial

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BOSTON (Reuters) - Two Harvard teaching hospitals and a prominent Alzheimer's disease researcher accused of using falsified data to obtain a government research grant are set to stand trial after a federal appeals court said this week that a lower court erred when it dismissed the case.

The lawsuit accuses Marilyn Albert, a former professor of psychiatry at Harvard Medical School, and Massachusetts General Hospital (MGH), where she was conducting research, of submitting a grant application based on manipulated data.

The data showed results from a trial were scientifically significant when in fact they were not, according to the lawsuit.

Brigham and Women's Hospital, which collaborated on the research, is also a defendant in the case. The lawsuit was brought in 2006 under the False Claims Act, a 150-year-old federal law designed to recover government funds appropriated through fraud.

This is the first time a lawsuit dealing with alleged scientific fraud has been allowed to progress to trial under the False Claims Act, according to Michael Kohn, a lawyer with Kohn, Kohn & Colapinto in Washington, D.C.

Kohn represents the whistle-blower in the case, Kenneth Jones, a former statistician at Massachusetts General Hospital, who filed suit in 2006 claiming the defendants violated the act by including false statements in a $15 million grant application to the National Institutes of Health (NIH).

The case was dismissed in the lower court three days before it was due to go to trial. Barring settlement, a new trial could begin later this year in U.S. District Court in Boston, Kohn said.

If the defendants are found guilty, they could pay as much as $45 million to the U.S. government. By law, whistle-blowers in such cases receive 15 percent to 30 percent of funds recovered.

Albert, who is now director of the Division of Cognitive Neuroscience at Johns Hopkins University School of Medicine, declined to comment except to say in an email: "I am confident that there was no misconduct involved."

Both hospitals said they are confident the researchers acted appropriately and according to the highest standards of scientific integrity.

"While it is disappointing that additional time and resources will have to be devoted to defending the institution and its investigators, the MGH remains confident that the resolution of the case will show that the allegations are without merit," Massachusetts General said in a statement.

Brigham and Women's responded with an identical statement.

INFLUENTIAL RESEARCH

Albert's research was part of an ongoing investigation into the structure of the brain as it progresses toward Alzheimer's disease. She specifically hoped to show that it might be possible to predict, years in advance, who might be destined to develop the disease, based on measurements taken over time of certain regions of the brain.

The results of the trial were published in the scientific journal Annals of Neurology in April 2000 and, according to Jones, proved extremely influential.

"The data appeared to confirm what had been suspected by some very prominent scientists, which is that Alzheimer's disease is associated with decreased blood flow to the brain," Jones said in an interview on Thursday. "The MRIs showed the volume of certain parts of the brain was decreasing in the people who were sick."

There are multiple theories about the cause of Alzheimer's disease.

In March 2001, Jones discovered what he believed to be anomalies in the research, specifically in data produced by one of the researchers, Ronald Killiany. The lawsuit alleges that Killiany revised his initial MRI measurements to prove the hypothesis of the trial.

Killiany, now an associate professor at Boston University School of Medicine, did not return a phone call or email seeking comment. Kohn said he was not named as a defendant. In retrospect, Kohn said, "He probably should have been."

Jones took his concerns to Albert, who authorized an investigation into the matter by Killiany's boss, Mark Moss. She declined to appoint an independent investigator, as requested by Jones, according to the lawsuit.

Moss concluded that Killiany's second set of measurements was more accurate than the initial set. Albert accepted Moss's conclusion and proceeded to apply for an NIH grant in November 2001, according to the lawsuit.

The defense argued before the appeals court that it would not have been unusual or inappropriate for Killiany to re-measure patient brain scans as long as he remained blind to the clinical status of the participants, and that this was a matter for scientific debate.

This argument was accepted when the case was initially heard by the lower court in the United States District Court for the District of Massachusetts. On that basis, it dismissed the case in October 2010. Kohn said the court ruled that scientific fraud could not be brought under the False Claims Act, since the case related to a scientific dispute, not fraud.

The appeals court, however, rejected the argument, saying, "We disagree that the creation of the data in question was necessarily a matter of scientific judgment."

The court noted that the lower court's determination "misses the point that the various results produced in this case were obtained by one scientist purportedly using the same protocol."

The government's Office of Research Integrity declined to say whether it is investigating the case.

Jones said he hopes the trial will shed light on the issue of scientific misconduct.

"My interest is in correcting the science and bringing this academic cheating to light," he said, "and maybe sending a message saying, 'You're being watched, and you shouldn't do it.'"

The case is: U.S. ex rel. Jones v. Brigham and Women's Hospital, et al, 1st U.S. Circuit Court of Appeals, No: 10-2301.

(Editing by Michele Gershberg and Douglas Royalty)