Another prestigious award came for the film “Dubrovnik & Time” from Poland, with the 11th FilmAT – Film, Art & Tourism Festival Poland, which is one of the most important film festivals in the field of tourism, ecology and art in the world.The promotional tourist film DUBROVNIK & TIME has won as many as eight important awards since its presentation at the beginning of March. The last one was awarded to him in the Polish city of Lublin, at the eleventh FilmAT festival as the best short (less than 5 minutes) promotional film about the city. The screening of the film “Dubrovnik & Time” arouses the enthusiasm of the viewers with each screening, and the confirmation of its quality has so far won important awards at international film festivals.DUBROVNIK TOURISM 2016 from Readmore Films on Vimeo.
Share Email Pinterest Share on Facebook LinkedIn More people may be diagnosed due to a broader definition of autism and better efforts in diagnosis, but a true increase in the disorder cannot be ruled out, according to the U.S. Centers for Disease Control. Lifestyle change is one potential factor out of many possible causes of autism.‘One thing that’s driving a lot of general physiological changes in people is changes in the diet,’ says the study’s corresponding author Pamela Maher, a senior staff scientist in the laboratory of professor David Schubert at the Salk Institute for Biological Studies.In the new study, the Salk scientists used a mouse model of autism — an inbred strain of mouse previously found to display autism-like symptoms — to ask whether lowering the level of dicarbonyl methylglyoxal (a common byproduct of sugar metabolism) could alleviate symptoms of autism in the animals.The scientists fed pregnant mice either the high or low glycemic index diet and kept their offspring on the same diet after birth and weaning, because their brains are still forming crucial connections.The researchers then used a battery of behavioral and biochemical tests to study the mice after weaning. The two groups of animals consumed the same number of calories and were identical in weight. But mice that ate a high-glycemic index diet showed all of the expected behavioral symptoms of autism. Their social interactions were impaired, they repeated actions that served no apparent purpose, and they groomed extensively.The mouse models of autism on a normal lab diet (with a medium glycemic index) are already known to generate fewer new neurons, and some of their existing cells and neuronal connections are abnormal compared with those of normal mice.Intriguingly, in the new study, the brains of mice modeling autism that were fed the high-glycemic index diet had drastically less doublecortin, a protein indicator of newly developing neurons, compared to predisposed mice on the low-glycemic index diet. The deficiency was especially obvious in a part of the brain that controls memory.In addition, the brains of the high-glycemic index diet mice appeared to have greater numbers of activated microglia, the resident immune cells of the brain. Their brains also expressed more genes associated with inflammation, compared to the mice fed the low-glycemic index diet.Other studies of human mothers and their children with autism have implicated the activation of the immune system. For the most part, these studies have focused on infection, which causes a bout of inflammation — as opposed to a high-glycemic index diet, which causes chronic, low-level inflammation, Maher says.The new study found that the diet might directly influence the ecosystem of bacteria in the gut. More complex starches are broken down by bacteria that live in the lower part of the gut, the large intestine. The group saw some evidence of that in the blood, detecting metabolites that could only have come from the gut in larger amounts in the animals fed the high-glycemic index diet.‘We were really surprised when we found molecules in the blood that others had reported could only be generated by gut bacteria,’ Maher says. ‘There were big differences in some of these compounds between the two diets.’The group plans to analyze the gut bacteria, and its potential link with features of autism, more directly. They also hope to better understand the role of inflammation in the ability to generate new neurons.Lastly, they plan to vary the timing of exposure to the various diets in the mouse model of autism, by, for example, giving pregnant mice a high-glycemic index diet and then keeping their pups on a normal diet. Bread, cereal and other sugary processed foods cause rapid spikes and subsequent crashes in blood sugar. In contrast, diets made up of vegetables, fruits and whole grains are healthier, in part because they take longer to digest and keep us more even-keeled.New research in a mouse model of autism showed that such low glycemic index diets, similar to the plans that people with diabetes follow to keep their blood sugar in check, reduced symptoms of the disorder in mice. Although preliminary and not yet tested in humans, the findings, published June 9 in the journal Molecular Psychiatry, might offer clues to understanding one potential cause of autism.The number of people diagnosed with autism — a spectrum of disorders characterized by social avoidance, repetitive behaviors and difficulty communicating — has risen dramatically over the past two decades for reasons that are unclear. Share on Twitter
Share Share on Facebook Pinterest The discovery is encouraging as it offers an avenue to track the progression of Alzheimer’s disease over time, but it also generates a lot of questions. Researchers want to know how best to boost NPTX2 levels and if there is an added benefit. They were struck by a trend in the data that points to a possible answer. Study participants with more years of education showed higher levels of the protein. Willette says people with complex jobs or who stay mentally and socially active could see similar benefits, supporting the notion of “use it or lose it.”“You’re keeping the machinery going,” Willette said. “It makes sense that the more time spent intensely focused on learning, the more your brain is trained to process information and that doesn’t go away. That intense kind of learning seems to make your brain stronger.”Good vs. bad proteinsWillette and Swanson used data from the Alzheimer’s Disease Neuroimaging Initiative to assess which aspects of the immune system were most relevant to tracking Alzheimer’s disease progression. They consistently found two proteins (NPTX2 and Chitinase-3-like-protein-1, or C3LP1) that predicted aspects of the disease. Among 285 older adults, they examined memory performance at baseline, six months, one year and two years. At the beginning of the study, 86 participants had normal brain function, 135 expressed mild cognitive impairment (the precursor to Alzheimer’s), and 64 had Alzheimer’s disease.ISU researchers also focused their attention on the medial temporal lobe, an area of the brain that shows the first signs of memory loss or cognitive decline in Alzheimer’s disease. While C3LP1 modestly predicted atrophy in the medial temporal lobe, it did not track memory decline over time, researchers said. After two years, the presence of NPTX2 explained 56 percent of the fluctuation in memory loss and 29 percent of medial temporal lobe volume.Willette and Swanson say they were somewhat surprised by the comparative results. They expected C3LP1, which causes brain inflammation and is thought to degrade the brain and memory, to be a stronger indicator. However, the memory forming benefits of NPTX2 proved to be consistently significant during the two years that researchers tracked memory decline and medial temporal lobe atrophy.“We see this as a promising biomarker that affects a lot of key aspects of Alzheimer’s disease,” Swanson said. “It’s a revolutionary approach and we’re looking at it in a more holistic way, rather than a reductionist viewpoint, to understand how the immune system and brain are connected.”Willette added, “With this disease you have to be comprehensive. There are so many aspects of our environment, our lifestyle, our immune system that influence the degree to which you’re at risk for Alzheimer’s disease.” LinkedIn Share on Twitter Iowa State University researchers have identified a protein essential for building memories that appears to predict the progression of memory loss and brain atrophy in Alzheimer’s patients.Auriel Willette, an assistant professor of food science and human nutrition; and Ashley Swanson, a graduate research assistant, say the findings also suggest there is a link between brain activity and the presence of the protein neuronal pentraxin-2, or NPTX2. The research, published in the journal Brain, Behavior and Immunity, found a correlation between higher levels of NPTX2 and better memory and more brain volume. Lower levels of the protein were associated with diminished memory and less volume.“NPTX2 seems to exert a protective effect,” Swanson said. “The more you have, the less brain atrophy and better memory you have over time.” Email
Pinterest Share on Facebook LinkedIn Share Email Share on Twitter Patients were randomized to receive active medication duloxetine, a selective serotonin and norepinephrine reuptake inhibitor, or placebo. During the trial, patients receiving medication experienced significant improvement of symptoms compared with patients receiving placebo. In medication-treated patients, cortical thickness declined toward values found in healthy volunteers while placebo-treated patients showed a slight thickening of the cortex. According to Bansal, a researcher at CHLA and professor of pediatrics at the Keck School of Medicine of USC, this finding suggests that placebo-treated patients continue to require compensation for their ongoing symptoms.“Although this study was conducted in adults, the methodology developed – pairing a randomized controlled trial with MRI scanning – can be applied to many other populations in both children and adults,” said Bansal. “Also, our observations of neuroplasticity suggest new biological targets for treatment of persons with neuropsychiatric disorders.” A study led by Ravi Bansal, PhD, and Bradley S. Peterson, MD, of The Saban Research Institute of Children’s Hospital Los Angeles, has found structural differences in the cerebral cortex of patients with depression and that these differences normalize with appropriate medication. The study, published in Molecular Psychiatry on March 7, is the first to report within the context of a randomized, controlled trial, the presence of structural changes in the cerebral cortex during medication treatment for depression and the first to provide in vivo evidence for the presence of anatomical neuroplasticity in human brain.“Our findings suggest that thickening of the cerebral cortex is a compensatory, neuroplastic response that helps to reduce the severity of depressive symptoms,” said Peterson, director of the Institute of the Developing Mind at CHLA and professor of pediatrics and psychiatry at the Keck School of Medicine of the University of Southern California. “Patients off medication have a thickened cortex, and the thicker it is, the fewer the symptoms they have. Treatment with medication then reduces the severity of symptoms, which in turn reduces the need for biological compensation in the brain – so that their cortex becomes thinner, reaching thickness values similar to those in healthy volunteers.”The investigators acquired anatomical brain scans at baseline and again at the end of the 10-week study period for 41 patients with chronic depression, while 39 healthy volunteers were scanned once. This study was conducted with adult patients treated at Columbia University, when Peterson and Bansal were faculty members.
Pinterest Share on Facebook LinkedIn 512 people took part in a series of studies conducted by Jason Tsukahara, Tyler Harrison & Randall Engle (Gerogia Institute of Technology), that investigated the relationship between resting pupil size and working memory (part of short term memory associated with immediate processing) capacity and fluid intelligence (the ability to think abstractly and problem solve). Pupils were measured by eye tracking units whilst participants carried out tasks relating to memory and fluid intelligence.The results of the studies revealed that there are huge differences in resting pupil size in individuals with high cognitive ability compared to those with low cognitive ability. In some cases these differences were even visible to the naked eye. Additionally, differences in pupil size are maintained even when people are doing a task that requires mental exertion. Even factors like age and drug abuse (which are related to pupil size) did not account for the relationship between fluid intelligence and resting pupil size, meaning that determining resting pupil size could be an effective measure of an individual’s intelligence and cognitive capacity.Although the findings of this study show that resting pupil size has the potential to help us understand mental processing, the authors state that ‘baseline pupil size is only reasonably formed speculation’. This means that further research is needed to fully understand the individual differences in resting pupil size. Email Share Share on Twitter Resting pupil size could be a predictor of cognitive ability in humans, according to a study recently published in Cognitive Psychology.It is established that pupil size reflects more than simply the amount of light entering the eye. However, it was previously thought that pupil size was too crude a measure of brain activity. More recently though, the discovery that activity in an area of the brain known as the locus coeruleus results in changes to pupil size has opened the possibility that pupil size could be a useful indicator of neural processing.The locus coeruleus is a part of the brainstem with connections across the rest of the brain, including the prefrontal cortex, which plays a crucial role in cognitive abilities such as memory and intelligence. The locus coeruleus is the main source of neurotransmitter, norepinephrine in the central nervous system, which amongst other things regulates cognitive activity in areas such as the prefrontal cortex. Therefore, it is possible that pupil size may actually be a valuable reflection of neural activity which can be used to determine differences in cognitive ability in humans.
Share on Facebook Share Pinterest Email LinkedIn Share on Twitter Two landmark publications with one or more co-authors from the University of Cincinnati Gardner Neuroscience Institute outline a transformative approach to defining, studying and treating Parkinson’s disease. Rather than approaching Parkinson’s disease as a single entity, the international cadre of researchers advocates targeting therapies to distinct “nodes or clusters” of patients based on specific symptoms or molecular features of their disease.Alberto Espay, MD, associate professor in the Department of Neurology and Rehabilitation Medicine at the UC College of Medicine and director of the James J. and Joan A. Gardner Family Center for Parkinson’s Disease and Movement Disorders, is lead author of the publications, which recently appeared online in the journals Nature Reviews Neurology and Movement Disorders.“The time has come to ask what we should be doing differently,” Espay says. “Medical science has made a global investment of $23 billion in therapies with the promise to slow down the progression of Parkinson’s disease, and the 17 completed phase III clinical trials have yielded little more than disappointment. We need to ask whether the growing number of failed trials might be explained by our single-target and single-disease approach to drug development.”Espay and his colleagues theorize that Parkinson’s is not one disease but rather several diseases when considered from genetic and molecular perspectives. They acknowledge that viewing Parkinson’s as a single disorder that predominantly involves dopamine-neuron degeneration has been useful in the development of treatments for symptoms, such as tremor and unstable walking, that touch the vast majority of patients. At the same time, this view has yet to deliver a therapy that is effective in slowing, modifying or curing Parkinson’s. One important reason, Espay says, could be that promising molecular therapies have been tested in large clinical trials of people who share the diagnosis of Parkinson’s, but not to the specific disease subtype most likely to benefit.The researchers advocate a “precision medicine” approach that is rooted in systems biology, an inter-disciplinary study that focuses on the complex interactions of biological systems.“Looking at the disease from a systems biology perspective allows us to recognize that our patients can be divided into subtypes based on genetic, biological and molecular abnormalities,” Espay says. “As a result, they will respond differently to different therapies.”Neurologists have long observed the many faces of Parkinson’s in their patients. Some progress rapidly in their disease, some slowly. Some develop dementia relatively early, while others do not.Tests have also revealed that patients develop deposits of alpha-synuclein, a protein, to varying degrees in the brain, colon, heart, skin, and olfactory bulb. But while these deposits have been thought to be common denominators in most individuals with Parkinson’s, they may represent byproducts of a range of biological abnormalities and may not be the best targets of therapy. “Chasing this tail could prove an elusive target,” Espay says.Toward an Ideal Set of BiomarkersEspay and his colleagues say the field must work to develop an ideal set of biomarkers. Their sobering conclusion comes after an investment of $45 million by the Michael J. Fox Foundation in the Parkinson’s Progression Markers Initiative (PPMI). Espay, the site leader for Cincinnati’s portion of the 33-site study, had hoped the effort would help researchers discover biomarkers that would pinpoint underlying disease processes.The ideal approach, Espay and his co-authors write, would start with “an assessment of biological processes” in large populations of aging individuals. The assessments would capture brain scans, genetic profiles and other biological measurements of healthy and unhealthy individuals over time. Abnormal signals within each of these biological measurements would then be traced to the group of people from which they emerge. In so doing, the field would develop “unbiased biomarkers” that drive the creation of specific disease subtypes.“This process is the reverse of what we have today, with biomarkers being validated by anchoring them to the patient’s observable clinical features, or phenotypes,” Espay says.Espay has likened the situation to an earlier period in oncology, when researchers sought “the cure for cancer.” Over a period of decades, cancer researchers evolved away from that blanket focus to an understanding of cancer’s profound complexity. They learned to assess a cancer’s molecular profile and to target its unique mutation or vulnerability. In so doing they ushered in the age of precision medicine – the matching of drugs to disease subtypes.“The neurologist of the future would look very much like the oncologist of the present,” Espay says. “The diagnosis of Parkinson’s disease will be complete only when a biomarker profiling is capable of identifying the molecular subtypes of disease and suggest a disease-modifying treatment to apply.”Co-authors of the Nature Reviews publication are Patrik Brundin, MD, PhD, of the Van Andel Research Institute in Grand Rapids, Michigan, and Anthony Lang, MD, of the University of Toronto. Co-authors of the Movement Disorders article include Aristide Merola, MD, PhD, assistant professor of neurology and a member of the UC Gardner Center, and Daniel Woo, MD, professor of neurology and a member of the UC Comprehensive Stroke Center.Espay and co-investigator Hilary Perez, PhD, clinical instructor and research coordinator at the Gardner Center, will lead UC’s future efforts in biomarker development in collaboration with the Parkinson Study Group, the largest not-for-profit scientific network of Parkinson centers in North America.
A study of incarcerated juvenile sex offenders suggests that psychological abuse in childhood may have uniquely damaging effects on mental health.The findings, which appears in the Archives of Sexual Behavior, shed light on the roots of hypersexuality, which has been found to be a predictor of recidivism.“I have been doing research on various aspects of sexual aggression for the last four decades. It is clear that primary prevention is the optimal intervention strategy for reducing sexual violence,” explained Raymond A. Knight, the corresponding author of the study and professor emeritus of human relations at Brandeis University. Share Pinterest “Consequently, in my laboratory we have been focusing on identifying the developmental antecedents of various risk factors for sexual aggression. Knowledge of such antecedents is essential for designing and implementing prevention strategies.”In the study, the researchers surveyed 307 male juveniles who were about 16 years old on average and had committed at least one serious sexual crime. The participants completed assessments of abuse and other adverse childhood experiences.The researchers found those who reported higher levels of psychological abuse by a male caregiver tended to also report more problematic and excessive sexual thoughts and behaviors. The same was true of those who reported more severe sexual abuse in childhood. “Psychological abuse, especially in this case of a father toward his son, is a powerful predictor of hypersexuality and indeed in other studies from our laboratory of other prequels to sexual and nonsexual violence. It requires enhanced research scrutiny to unpack the potential causal components it encompasses,” Knight told PsyPost.Like all research, the study includes some limitations.“This is a retrospective, not a prospective study. The youths are reporting recent past experiences and behavior. All the methodological problems with such a research strategy apply,” Knight explained.“Nonetheless, we have replicated these findings with an adult sample, indicating their cross-sample consistency. Prospective studies of psychological and sexual abuse aimed at unraveling the essential causal mechanisms involved in each and examining their consequences are essential.”The study, “The Relation of Childhood Abuse Experiences to Problematic Sexual Behaviors in Male Youths Who Have Sexually Offended“, was authored by Kathryn A. Davis and Raymond A. Knight. Share on Facebook Email Share on Twitter LinkedIn
LinkedIn Share on Facebook Pinterest Share “What struck me most was how some people around me responded to those scenes of innocent victimization not with empathy, but with victim blaming and derogation. I was then arrested and tortured myself and was further shocked when, after being released, members of my own family blamed me for bringing this to myself. Consequently, I became curious about what factors play into how people respond to innocent victims.”In the study, 100 undergraduate students watched five short videos showing the suffering of innocent victims, such as a scene depicting a call from a 9/11 victim before the collapse of the Twin Towers. After watching each video, the participants then completed assessments of victim derogation and negative emotions. After watching all five videos, the participants completed questionnaires on just-world beliefs and emotion avoidance.The researchers found that higher levels of negative emotions were associated with reduced victim derogation among participants with a lower tendency to avoid their emotions. “Our findings suggest that when individuals empathize with victims by vicariously experiencing their distress, they may be less likely to derogate them,” the researchers wrote in their study.Beliefs in a just world, on the other hand, were unrelated to victim derogation. In other words, people who agreed with statements such as “People usually receive the outcomes that they deserve” were not more likely to derogate the victims.“For more than 5 decades, the phenomena of victim blaming and derogation have been explained with just-world theory, which posits that beliefs about a just-world underlie these phenomena. The findings in our study challenge just-world theory and suggest that emotional factors such as empathy and emotion avoidance may play a more important role than beliefs in explaining victim blaming,” Ash told PsyPost.But the study — like all research — includes some limitations.“This is a preliminary study. It was cross-sectional and correlational in nature and any causal inferences should be made with caution. Future directions include experimentally manipulating empathy and emotion avoidance to further clarify the roles of negative emotions and emotion avoidance in victim derogation,” Ash explained.“The study suggests an important methodological flaw in the way psychological studies are conducted. Previous studies on victim-blaming and derogation had used written vignettes that may not have approximated real-life very well. By contrast, our study shows that when we used emotionally-arousing videos that more accurately simulated real-life, just-world beliefs had no effect on victim-blaming/derogation.”“Our findings suggest that, given the empirical evidence showing that emotions strongly contribute to behavior, psychological studies should use more emotionally-arousing stimuli, include emotional variables in their statistical models, and strive to approximate real-life as much as possible,” Ash added.The study, “Negative emotions and emotion avoidance in victim derogation“, was authored by Jude Ash and K. Lira Yoon.(Photo credit: Anthony Gale) New research published in Personality and Individual Differences provides evidence that negative emotions and emotion avoidance play an important role in victim derogation.Victim derogation describes the phenomenon in which innocent victims of suffering are perceived as having less positive traits. Previous theories have held that this negative bias towards victims is used to maintain the belief that the world is fundamentally fair. But the new study suggest that this is not always the case.“In 2011, I was involved in the Syrian nonviolent movement calling for democracy and human rights. During the uprising, videos flooded YouTube showing unarmed protestors shot in cold blood and children tortured to death,” said study author Jude Ash, a PhD student at the University of Notre Dame Share on Twitter Email
New Hampshire site of anthrax exposure is reopenedThe Waysmeet Center at the University of New Hampshire has been disinfected and was reopened Apr 16, according to a Foster’s Daily Democrat report. The center is home to United Campus Ministry and the apparent source of spores that caused gastrointestinal anthrax in a woman who attended a drum circle event there last December. “We’re absolutely certain it’s safe to enter,” said Dr. Jodie Dionne-Odom, New Hampshire’s deputy state epidemiologist. The patient recently returned home from the hospital and is “walking around and talking and able to answer questions,” Dionne-Odom said, adding that her long-term prognosis is uncertain. Cleanup professionals scrubbed the entire building between March 22 and April 14, finding Bacillus anthracis spores, which cause anthrax, throughout the building, including on electrical outlets and two animal-hide drumheads. The cleanup cost $50,000, and the spores were ruled to be of natural origin. Officials believe the woman swallowed anthrax spores during a “brief aerosolization” event amid “vigorous drumming,” Dionne-Odom said.Apr 17 Foster’s Daily Democrat story Study: Raw chicken identified as source of Listeria at plantA recent 21-month study by Agricultural Research Service (ARS) scientists at the University of Georgia concluded that incoming raw poultry rather than workers or the environment is the main source of Listeria monocytogenes contamination in commercial cooking plants. The test site was a brand-new cooking facility free of Listeria when first opened. Samples were taken regularly during the study period from potential sources of contamination, including soil and water near the facility, floors in various parts of the plant, incoming air, and raw meat. Listeria was found in floor drains within 4 months of the start of operations. The only tested source that was consistently positive for the organism was the raw meat. Study results can help facilities focus their sanitation efforts to reduce cross-contamination. The study was published in the Journal of Food Protection.Study abstractApr 19 ARS news story Apr 19, 2010 Plague, hantavirus alert issued for New MexicoPeople in New Mexico have been warned by state health officials to be on the alert for plague and hantavirus in animals this spring after several confirmed cases of plague were reported in cats and dogs. Plague can spread to pets when they eat infected rodents or are bitten by fleas from the rodents. The disease can then spread to humans through direct contact with infected pets or bites from the pets’ fleas. Humans can contract hantavirus through breathing in aerosolized virus from rodent urine, droppings, or saliva. The main carrier is deer mice. Among preventive steps are avoidance of sick and dead rodents and rabbits as well as their habitats, keeping pets from roaming and hunting and use of flea-control products, trapping mice and keeping them out of homes and cabins, not disturbing rodent nests and droppings without good ventilation, and seeing a vet if pets show fever, lethargy, or loss of appetite. Plague symptoms in humans include fever, chills, headache, weakness, and swelling of lymph nodes; early hantavirus symptoms include fever and muscle aches.Apr 16 release from New Mexico Department of Health
Researchers find possible cause of severe second dengue infectionsInfectious disease experts have long puzzled why people who are infected for a second time with a different strain of dengue virus have a more severe illness course, but new findings in the latest issue of Science may provide a clue. Researchers from Imperial College of London report that they have identified a set of antibodies called precursor membrane (prM) protein that “awaken” during the first infection and help infect more cells during the second infection, the college said in a press release. Dr Gavin Screaton, the study’s lead author, said in the statement that the findings will help with vaccine development, because scientists can avoid including prM in any future vaccines. “Our new research gives us some key information about what is and what is not likely to work when trying to combat the dengue virus,” he said. “We hope that our findings will bring scientists one step closer to creating an effective vaccine.” Dengue fever is a mosquito-borne viral disease found in tropical and subtropical regions. The virus occurs in four serotypes, and infection with one induces immunity only to that serotype. A second infection with a different serotype increases a person’s risk for dengue hemorrhagic fever, which involves bleeding and the possibility of life-threatening shock.May 6 Imperial College of London press releaseMay 7 Science abstract May 7, 2010 WHO reports progress toward eradicating guinea worm diseaseThe World Health Organization (WHO) said today that though the world won’t meet the goal of eradicating the parasitic disease dracunculiasis (guinea worm disease) this year, significant progress has been made, with disease transmission interrupted in 8 of the 12 African countries where it is endemic. The WHO published a status report on dracunculiasis in today’s issue of its Weekly Epidemiologic Record. The disease is spread by drinking water that contains fleas that have ingested Dracunculus larvae, the WHO said. In humans, the larvae invade body tissues, where they grow before emerging through the skin. There is no vaccine or treatment, and the only prevention is protecting and filtering water sources. In 2004 at the World Health Assembly countries signed a declaration to eradicate the disease by 2010. In addition to the eight countries that have interrupted transmission, three more are close to reaching that goal, the WHO said. Sudan, with the world’s highest number of cases is the only country in which transmission interruption doesn’t appear to be a realistic near-term goal. The WHO said the passing of the eradication target date signals a need to reassess the situation and move forward with new efforts. It added that elimination is still a realistic goal.May 7 WHO Weekly Epidemiologic Record reportWHO dracunculiasis background