Health Meaning

Cataracts cloud the eyes of tens of millions of people worldwide and nearly 17.2% of Americans over 40 years now, the only treatment is surgery or scalpels cut -Lasers molecular grout that builds in the eye cataracts develop, and surgeons sometimes replace the lens. But now a team of scientists and ophthalmologists tested a solution in dogs that may be able to dissolve the cataract right out of the lens of the eye. And the solution is itself a solution :. Eye drops containing steroids

Although scientists do not fully understand how cataracts form, they know that the "fog" often seen by patients is a glob of broken proteins, glued together in a dysfunctional bunch . When health, these proteins, called crystalline, help eye lenses keep its structure and transparency. But like humans and animals alike older, the Crystalline proteins begin to disintegrate and lose their ability to function. Then they agglutinate and form a sheathlike obstruction in the lens, causing vision signature "wet glass" that accompanies the cataract.

Coming up with an alternative to the surgery was difficult. Scientists have been hunting for years to mutations in the Crystalline proteins that could provide new opportunities and open the way to another therapy. Now, it looks like a team led by the University of California (UC), San Diego, molecular biologist Ling Zhao was able to do that. His team came up with the idea of ​​eye drops after finding that children with an inherited form of cataract shared a mutation that has stopped production of lanosterol, a major steroid in the body. When their parents are not the same mutation, adults lanosterol product and had no cataracts

Thus, the researchers wondered :. What if lanosterol helped prevent or reduce cataract? The team tested a lanosterol solution loaded in three separate experiments. First, they used human lens cells to test the effectiveness lanosterol decreased cataracts laboratory models. They have seen a significant decline. They then progressed to rabbits suffering from cataracts. At the end of the experience of 6 days, 11 of the 13 rabbits were parties to have serious or significant cataracts at a slight cataract or no cataracts. Finally, the team moved to dogs, using a group of seven, including black Labs, Queensland Heelers and Miniature Pinschers with cataracts naturally. Dogs have reacted as the researchers hoped lanosterol solution, which was given in the form of two eye injections and eye drops. lenses of dogs showed the same type of dissolution because the cells of the human lens and rabbits.

The improvement was remarkable, researchers could tell just by looking dog eye cataracts decreased. But the exact mechanism of how manages lanosterol to disperse the mass of proteins remains unknown.

"This is really complete and convincing the stronger paper that I saw of its kind in a decade," said Jonathan King, a molecular biologist at the Massachusetts Institute of Technology in Cambridge not affiliated in the study. He studied proteins cataract since 00. "They discovered the phenomena, then follow up with all the experiences that you should do that is biologically relevant as you can get."

Ruben Abagyan, co-author of the paper and a molecular biologist at UC San Diego, is eager to see what the lanosterol drops may dissolve following. "I think the natural next step is looking to translate in humans," he said. "There is nothing more exciting than that."

It has long been known that obesity women more prone to cancer brands breast, but the reasons are not clear. The researchers found that the tissue surrounding the breast cells is "more rigid" in mice and obese women, and that this difference of tissues in rodents spurs the growth of cancer cells. For women, the work suggests, weight loss can reshape fatty tissue and reduce the risk of cancer. Moreover, the growing practice of using fat from obese women for reconstructive surgery within them may present a risk which had been neglected until now.

Obesity is associated usually with cancer, but the link with breast cancer is particularly striking: In large recent study, the most overweight women had a risk 58% higher than normal weight women. One explanation is that fat tissue produces estrogen, which can fuel the growth of breast cancer cells after menopause, when the ovaries stop producing estrogen. But the mechanics of the scaffolding that surrounds the cells it within the extracellular matrix, may also matter.

Mice recent studies have found that a more rigid extracellular matrix triggers the production of proteins that promote cell growth of precancerous breast cancer. This may help explain why women with dense breasts are also at higher risk for breast cancer. Other studies have shown that when people become obese, their fat tissue tends to accumulate fibrous tissue scarlike pockets.

These studies did not address directly whether these fibrous pockets affect the local stiffness of the breast tissue, and if these changes lead to cancer growth. To explore this question, a team led by Cornell University biomedical engineer Claudia Fischbach first showed that female mice that were obese because of genetic or a diet high in fat, have more fibrous mammary fat pads with collagen fibers straighter than those observed in lean mice (see image). Mechanical tests have shown that straight fibers reflect more rigid extracellular matrix between breast cells. The researchers also found a surplus of myofibroblasts, a type of cell involved in wound healing that form the structure of collagen and other matrix proteins. When Cornell team human cells in breast cancer culture matrix filed by fat cells of obese mice derivatives, cancer cells grew faster than they did on the matrix thinner mouse cells .

The researchers found similar structural differences in adipose tissue biopsies of the breast obese and lean women, they report today in Science Translational Medicine . The results suggest that the most rigid extracellular matrix pockets in the breasts of obese women contribute to tumor growth as well as more aggressive cancers, Fischbach said, "People always think that it is all about the soluble factors, chemical products. It is also about the interaction with the physical parameters "

The news was not all bad. When the team of Fischbach put obese mice on a diet, their mammary fat had fewer myofibroblasts, suggesting weight loss could make the fat of a woman structure more normal tissues and reduce her risk of breast cancer. at the same time, the study raises questions using clean grease from a woman also in his body to reconstruct breasts after mastectomy. the adipose tissue of obese women may increase the risk of a recurrent tumor, Fischbach suggests.

Biochemist Valerie Weaver of the University of California, San Francisco, who previous studies conducted between tissue stiffness and breast growth, called the paper "very important" because it is a new mechanism linking obesity with breast cancer. mammograms often can not detect dense tissue in obese women because it is hidden by fat cells, said Fischbach. Small local areas of rigid tissue found in the new study are particularly likely to fail, she added. Thus, new detection methods may be needed to diagnose these hotspots of potential cancer-promoting.

Since 1958, about 30 000 people worldwide, mostly children, were given hormone injections of human growth extracted from the pituitary gland of human corpses for treat their small size. The procedure was halted in 1985 when researchers found that a small percentage of the beneficiaries had received contaminated injections have been the development of Creutzfeldt-Jakob disease (CJD), a fatal neurodegenerative disease caused by poorly protein folded called prions.

Now, a new study of brain dead eight people who contracted CJD from these injections suggests that injections may also have spread amyloid-β, the neuron-clogging protein that is a feature of Alzheimer's disease. The study is the first evidence in humans that the amyloid-β could be transmitted through medical procedures such as brain surgery, the researchers said. Skeptics, however, note that the CJD prion often triggers unusual amyloid deposits; epidemiological studies, they say, found no link between the injections and an increased risk of developing Alzheimer's disease.

Outside of CJD and mad cow tied, kuru is perhaps the most famous prion disease. Endemic to Papua New Guinea and now essentially eradicated, kuru is transmitted by the ritual consumption of human brain tissue at funerals. Increasingly, however, scientists recognize that a number of other neurodegenerative diseases, including Alzheimer's disease, Huntington's disease and Parkinson's disease, also involve aberrant proteins that act as "seeds "in the brain. They turn otherwise normal protein fibers "break form more seeds, pause, and form more seeds," says John Collinge, a neuropathologist at University College London and lead author of the new study.

Still unknown Alzheimer's disease is the role of proteins such as amyloid-β and tau play in the misfolded disease, and whether they are transmitted by direct contact with the consumer or contaminated brain tissue. Although scientists have managed to induce amyloid-β transmission in rodents, these experiments relied on "massive" overexpression of the protein, said Samuel Gandy, neuropathologist at the medical School Icahn Mount Sinai in New York City. "Exhaustive" tent reproduce such transmission in primates have failed, he said, led many to doubt whether such propagation is possible.

in the current study, Collinge and colleagues examined brain tissue eight people aged 36 to 51, who died of CJD approximately 30 to 40 years after receiving the growth hormone injections. Four had an amyloid-β because pathologists treat moderate to severe in people with Alzheimer's, but they did not have a second type of protein, tau, which is considered an important feature of the disease as well, today, reports the online team Nature . Two had softer deposits, more unequal; it was free-amyloid. "It is a very unusual finding," said Collinge. "In this age group, you really do not see this kind of pathology, unless you have a genetic predisposition to Alzheimer's disease," none of them did, he said.

However, scientists have known since the 190s that prion protein that causes CJD can "cross-grain" amyloid-β, which causes abnormal deposits to form, and vice versa, said Gandy. In such small, observational study, it is impossible to determine whether CJD became the β-amyloid seen in the brain tissue of deceased or protein seeds subjects were transmitted by injection, he said. None of the subjects showed signs of tau, another protein associated with Alzheimer's disease, he and others point.

to explore the possibility that CJD, not the seeds of amyloid-β, was the culprit, Collinge and also examined the brains of 116 people colleagues with a range of prion diseases unrelated to hormone injections. They found little to no β-amyloid pathology in this group, suggesting that CJD alone was not responsible for the disease, they say. It is an "argument" in favor of the group, said Claudio Soto, a neuroscientist at the University of Texas Health Science Center at Houston. Since prions come in many different forms, however, it is still possible that beta-amyloid deposits found in the brains of injection beneficiaries were actually caused by CJD, whereas the controls were without plate he notes.

then Collinge's team plans to test for growth hormone vials archived original treatments to see if they can detect the amyloid β-protein "seeds." One obstacle, however, is that scientists do not know exactly what constitutes these seeds at the molecular level, Collinge said.

Though provocative, the new study can not answer the question of whether pathogenic amyloid-beta "seeds" can be transmitted from person to person through contaminated surgical instruments or blood, and Collinge Soto suitable. There is no epidemiological evidence to support this possibility, and an alarm on the contagiousness of Alzheimer's disease is premature, they said. Still, "which is something that should be studied," says Soto

* Updated, September 11, 9:30. Two authors of the study, John Collinge and Jonathan DF Wadsworth said a conflict of interest in the online version of the paper. Collinge is a director and both are shareholders of the D-Gen biopharmaceutical company Limited, which provides antibodies against prion proteins and developed a product prion decontamination, in collaboration with Du Pont Corporation.

West Africa was under the media spotlight this year and rightly after almost 11 000 people died in the largest Ebola outbreak ever recorded. But although the disease flickers in and out of the public consciousness, a new study shows that another killer was almost as deadly: snakebites. The study, published September 23 in PLoS Neglected Tropical Diseases , revealed that more than 4,000 people die each year in the same region because of poisonous snake bites. Besides crude mortality, snakebites result in more than 5000 amputations each year, filling up to 10% of hospital beds in some areas. The new findings are based on an analysis of the medical literature for 40 years. The researchers used the data to calculate the number of years lost due to illness, disability or early death of a proxy to estimate the total disease burden and found that 320,000 years of life disability adjusted lost every year in West Africa due to snake bites. This number exceeds the estimates for other tropical diseases, such as infection by nematodes and trypanosomiasis, which often receive more attention. The authors emphasize that antivenin, which is now extremely rare is effective both to treat and prevent snakebites and advocate for funding proportional to the high load.

prosthetic limbs can do wonders to restore lost function in some amputees, but one thing they can not do is to restore a precise sense of touch. Now, researchers report that one day in the not too distant, arms and legs may have an artificial sense of touch closely resembling the real thing. Using a two-layer thin flexible plastic, scientists have created new electronic sensors that send signals to the brain tissue of mice that mimic nerve messages of touch sensors in human skin.

Several research teams have long worked on the restoration of touch to people with prostheses. 2 years ago, for example, a group at Case Western Reserve University in Cleveland, Ohio, reported giving people with prosthetic hands a sense of touch by the wiring of the pressure sensors on the hands of the peripheral nerves in their arms.

However, although progress has restored a rudimentary sense of touch, sensors and signals are very different from those sent by mechanoreceptors, natural touch sensors into the skin. For starters, natural mechanoreceptors placed on what amounts to a digital signal. When they feel the pressure, they shoot a stream of nerve impulses; the higher the pressure, the higher the pulse frequency. But past tactile sensors have been analog devices, where more pressure produces a stronger electrical signal, instead of a more common current pulse. The electrical signals must then be sent to another processing chip which converts the force signal to a digital pulse stream that is only then sent to the peripheral nerves or the brain tissue.

Inspired by natural mechanoreceptors, researchers led by Zhenan Bao, a chemical engineer at Stanford University in Palo Alto, California, set to make sensors that churn out digital signals directly. The Bao group began by refining sensors that they first made 5 years ago. In this earlier work, the group designed tiny rubber pillars containing conductive carbon nanotubes of electricity, which were placed on a pair of electrodes together. When no pressure is applied, the rubber, which is an insulator prevents current from flowing between the two electrodes. But when touched, pressure crushes the pillars, pushing drivers nanotubes together to make a continuous electrical path and allowing current to flow. When the pressure is removed, the rubber pillars bounce back to their original shape.

In their current work, Bao and his colleagues turned their pillars inverted pyramids and refined their size so they were sensitive to a range of pressures from a light touch to a handful of steady hand. They also changed the configuration of the electrodes and adds another layer of flexible electronic devices, called ring oscillators, which convert the electrical signals coming out of touch sensitive pyramids to a stream of digital electrical impulses. The result is that, just like the natural signals mechanoreceptors-when more pressure is applied, oscillators prove pulses at a higher frequency.

Bao But the group does not stop there. The Stanford team also wanted to see if brain tissue could receive those signals. This usually done by inserting metal electrodes in the somatosensory cortex called animal and watch their response. But metal electrodes can quickly damage the natural brain tissue, making it impossible to study the transfer of signals over extended periods. So for their study, Bao's team decided to send electronic impulses from touch sensors to a diode that emits light, which turns them into a train of pulses of blue light. The Bao team and in partnership with Stanford colleagues, led by Karl Deisseroth, the genetically mouse somatosensory cortex tissue engineer to absorb blue light and fire in response. They sacrificed some of designed mice and isolated a slice of somatosensory cortex sensitive to light, which remained viable for several hours. Finally, they tested their tactile sensors and monitored if the mouse brain tissue received signals and fired in response. In today Science , they report that the neural tissue of the brain faithfully shooting modes from the touch sensor. This raises the hope that these sensors can possibly help restore a natural sense of touch to amputees, Bao said.

"It's great to see research in this direction, and this document is particularly impressive," said John Rogers, a chemist and expert in flexible electronics at the University of Illinois, Urbana-Champaign. Rogers and Bao notes however that give amputees a natural sense like touch has some way to go. Doctors, for example, will not be able to conceive of human brain tissue to receive light signals. This means that researchers will have to find other ways to transmit electrical signals of a prosthesis in the brain in a way that is safe and stable for long periods of time. Bao said she hopes to use the flexible organic electronics for this task as . well Finally, as these search son are woven together, it is likely to give people with dentures a whole new feel for their environment

(credit video. Bao research Group )

The West Nile virus (WNV), a pathogen transmitted by mosquitoes that can kill people and birds, is still rampant in North America, wiping out millions of birds each year across the continent, according to a new study. The research raises concerns about the long-term impacts of the disease, particularly on endangered species and endangered.

"It really is a fantastic study, but sobering," said Peter Marra, an ornithologist at the National Zoological Park, Smithsonian Institution in Washington, DC, who has not participated. "When combined with other threats such as land use, climate change, cats and buildings, it is not surprising that we see these declines in many bird species across United States."

Arrived in North America 16 years ago. Although it can infect and kill people, birds are the main host of the virus. But avian species in North America had never contracted WNV, and the novel pathogen spread across the continent in just 5 years, leaving millions of birds, finches jays to sparrows, dead in its wake. Previous studies have shown that factors such as climate and habitat affected how various bird species responded to the virus. For example, researchers have shown that urban birds seem more susceptible to the disease, although scientists do not yet know why.

To better understand these factors and to show the impact of WNV, a team of scientists analyzed 16 years of data from 1992 to 07 to more than 500 stations across the United States where birds are regularly imprisoned and banded. After 1999, these avian productivity Monitoring and Survivorship (MAPS) stations also began to check the birds for WNV, and so had the time records of where the disease has appeared at every station and in every case, and if the virus persists. Using this information, the scientists were able to determine if and how the virus first affected various bird populations, and if the numbers of birds have recovered or are still falling. (Scientists are not able to include MAPS data after 07 because they are not yet processed by volunteers and station personnel. However, researchers believe that the trends they have discovered not changed.) in total, they examined data over a quarter million birds of 49 species in 14 -in bird families, focusing on adults to more accurately determine the number of survivors.

Twenty-three of 49 species or 47% -were negatively affected by WNV, the report online today researchers in Proceedings of the National Academy of Sciences . They also found several striking models in the impact of the disease. Some first species suffered huge declines. Red-eyed Vireo ( Vireo olivaceus ) populations, for example, fell by about 29% when they first encountered the disease. Before WNV arrived, red-eyed vireo, a species that is widely distributed across the continent, had an estimated population of 130 million birds. Ultimately, nearly 37 million of these deaths probably vireo virus, scientists say. But the populations of this species are supported mass mortality in the first year of WNV hit. Their numbers subsequently recovered, which is the model that environmentalists disease waiting to see.

"It's like after a flu epidemic," said Ryan Harrigan, biologist of infectious diseases at the University of California, Los Angeles, and an author of the study. "Everyone builds immunity, and the impact tends to decline." Eleven of the 23 species affected in the study have experienced this type of recovery.

But the other 12 species are not so lucky. Their populations are still declining disease. "Seeing the persistence of the disease was a shock," says Harrigan. "We do not know why these species are unable to recover. It is alarming." For example, populations of vireo warbling ( Vireo gilvus ) fell 8.7% only when they have contracted WNV. But instead of recovering, populations of this species continued to decline annually by roughly the same percentage, a trend that scientists expect continued. "It is not just that he was a decrease of 8.7% a year; it is down 8.7% this population less next year and the year after, so the effect is compounded, "says Harrigan.

He and his colleagues believe that the WNV has killed more than 15 million of these vireo, nearly a third of their original population of 49 million. the thrush Swaainson ( Catharus ustulatus ), purple finch ( Carpodacus purpureus ), tufted titmouse (bicolor Baeolophus ), and Wrentit ( Chamaea fasciata ) were also affected.

to try to understand why some species are better than others to overcome the disease, the researchers compared the habitats "birds, to see if people in more urban landscapes had larger declines previous studies have suggested. Again, the results were mixed. Adult populations of 10 species, including the Spotted Towhee ( Pipilo maculatus ) and Song Sparrows ( Melospiza melodia ) have done very well in these habitats, perhaps because they have more food resources through human bird feeders provided. But 11 other species in those lost and probable urban areas continue to lose significant numbers of their adults.

The scientists also constructed a family tree of all species in the study to see if the closely related birds responded similarly to the virus. Again, the pattern was mixed. New sparrows and their close relatives, and generally vireos died off in the first year after contracting the virus, while the finches generally known persistent declines. Scientists say they do not yet know why some species are better than others in overcoming the disease.

"Is it because of differences in their immune systems or their habitats or the amount of exposure to [WNV]?" Says Harrigan. He and his colleagues are now looking more closely areas they have identified as those where some avian species are still dying of the disease to see if they can identify the reason.

other scientists expect that the study will lead similar investigations. "as with all good studies, it generates many new questions," says Staffan Bensch, an ecologist from animals to Lund University in Sweden, who wonders if the virus has benefited some songbird species by killing their avian predators, jays and crows.

Another mystery: WNV did not affect at least three species, the black-capped chickadee ( Parus atricapillus ), American robin ( Turdus migratorius ), and the wren house ( Troglodytes aedon ). "These species have gone straight through without any problems," says Harrigan. "How a species has no effect on this disease?"

Answering these questions will require more long-term data Type collected in MAPS stations, scientists say. "It will not be the last time we see a disease like this," warns Harrigan. And although the study did not focus on endangered species, all scientists fear the virus may be causing them further damage. "what is the effect on birds with smaller populations and ranges?" he said. Like many things about WNV, scientists not yet know. They only know that the disease and its effects on birds and North American people-are here to stay. Understanding more about how the virus affects birds and help them overcome this, so enjoy human, too, scientists say.

It can kill almost as many people as measles probably close to 0 000 in 2015, but few have heard of him, even among doctors in areas where deaths occur. It can occur decades after infection and in many different ways: as an abscess; as a fulminant infection of the blood with fever, headache, and pain; or as a lung infection with cough and chest pain which is easily confused with tuberculosis.

The obscure disease melioidosis and a research team now seems the alarm about this in a document that provides the first global estimates of the prevalence and the number of deaths it causes. "I am very pleased to see this published document," said Alfredo Torres, a microbiologist at the University of Texas Medical Branch in Galveston who was not involved in the work. "It is very clear that this disease has been underestimated and we must pay more attention to it. "

melioidosis is caused by the bacterium Burkholderia pseudomallei , which normally lives in the soil. People and a range of animals can be infected through skin lesions or during inhalation of contaminated dust or drinking contaminated water. The microbe can lead to an acute illness or slumber immediately before exploding in decades fledged melioidosis later, a trait that, once obtained the nickname of melioidosis is resistant to many antibiotics "Vietnamese time bomb." even when treated, up to half of patients can die.

discovered there are over a hundred years in the Burmese capital Yangon, then called Rangoon, the disease has traditionally been considered endemic to South Asia and the most northern regions of Australia . It is on the US list of potential bioterrorism agents ;. B pseudomallei can be aerosolized and had been studied as a bioweapon by the United States and other countries There was a growing recognition that melioidosis is more widespread than people had thought ... Recently, there have been case reports of several states in Africa and Latin America, for example Wherever people seemed to disease, they found, Torres said: "Brazil, India . It's the same story again and again. "in 2014, a survey conducted by the Centers for disease Control and Prevention (CDC) showed that the disease is endemic in parts of Puerto Rico as well.

To estimate the true global burden of disease, researcher Direk Limmathurotsakul Oxford Tropical Medicine Research Unit, Mahidol in Bangkok used a model that cuts the land mass of the planet in 8 million square 5 by 5 kilometers. From the data on soil characteristics, temperature and rainfall, and more than 22,000 cases of human or animal infections recorded during the last 100 years, he calculated how appropriate the ground in each square is B. pseudomallei . Using data from endemic areas known as Thailand, he then estimated the probability that the disease was really present. The model suggests that the disease is common in tropical areas, including 34 countries where it has never been reported, Limmathurotsakul and colleagues wrote online today Nature Microbiology . They estimate that there were 165,000 cases in 2015, including 89,000 deaths. As with any modeling effort, prediction comes with uncertainties, the authors give 68000-4100 case as a credible interval and 36,000 to 227,000 deaths.

"I have long suspected that B. pseudomallei is present in many countries where it was not previously identified," says David Speert, an infectious disease specialist at University of British Columbia in Vancouver, Canada. Not only is melioidosis often misdiagnosed as another illness, but the bacteria is also difficult to culture in the laboratory and difficult to identify. "Add to these problems the fact that B. pseudomallei is the most sensitive to extremely expensive antimicrobials and it is possible that appropriate therapy is not available, even if the diagnosis was made," said Speert .

In many countries where melioidosis has never been reported, clinicians have simply not learned to look. Limmathurotsakul and colleagues have prioritized 79 countries as needing their diagnostic capabilities of the disease and the enhanced microbe. "If the technicians are not aware that they need to test for it, they will just throw away culture because it looks like a contaminant of soil," says Limmathurotsakul.

Only melioidodis few cases occur in the US each year, almost all of them in people who have traveled to areas where the bacteria is endemic. But in a report last year summarizing the 08 data 2013, CDC noted that "three cases of melioidosis have occurred among US residents with no history or travel outside the United States or in areas where melioidosis is endemic, perhaps indicating sources not recognized exhibition in the United States. " Limmathurotsakul T model suggests that the more southern states have the appropriate environmental characteristics for the survival of the bacteria in the soil. "This sets the stage for subsequent infections if the body is to be introduced," says Speert. In fact, in November 2014 an outbreak occurred at Tulane Primate Research Center in Louisiana when the pathogen was spread from mice that were experimentally infected primates. Although the ground level around the fitness center is very small, the bacteria can settle in areas otheher in Lousiana, such as New Orleans, the authors write.

"This study is important," said Peter Hotez, dean of the national school of tropical medicine at Baylor College of medicine in Houston, Texas. "It confirms a high number of deaths in the world, so that melioidosis ranks with visceral leishmaniasis as one of the leading causes of death by a neglected tropical disease." Melioidosis is so neglected, however, it is even not on the list of the World Organisation of the health of neglected tropical diseases, said Torres. this must change, he said. "I really hope that this document will open the eyes of some people involved in health policy."

clusters of gold atoms can detect and kill cancer cells usually left behind after tumor removal surgery, according to a study of a new technical nanotechnology. For now, the approach has been tested in a mouse handle. But the researchers are designing a clinical trial that could begin testing in humans therapy over the next two years. If the technique proves effective in people, it could significantly improve the chances of cancer patients, especially in cases where surgical removal of an entire tumor is impossible.

When surgeons operate on patients with cancer, they do their best to eliminate every last diseased cell, because everything left behind can develop into new tumors or metastases in the body. Oncologists then usually follow up with surgery or radiation treatment or chemotherapy to increase the chance of eliminating all residual tumor cells. But this standard approach to fighting cancer is all but foolproof.

In recent years, doctors and scientists have turned to nanotechnology help. A pioneering approach over the last decade by researchers at Rice University in Houston, Texas and elsewhere has shown that atoms of gold clusters known as nanoparticles can serve as a powerful weapon against cells cancerous. solid tumor cancers generally have leaky blood vessels. Therefore, when gold nanoparticles are injected into the bloodstream, they tend to ooze out of the openings of the container and gather around tumors. To clean their environment, these cells then often engulf the nanoparticles. But once inside the cells, the nanoparticles can act as Trojan horses. When the researchers struck gold atoms with infrared laser light, which can travel through centimeters of tissue, the particles heat up and kill cancer cells.

Unfortunately, heating of the nanoparticle strategy has two problems, says Dmitri Lapotko, a physicist formerly with Rice and now head of the science of laser Masimo Corporation, a medical nanotechnology company in Irvine, California . The first is that some gold nanoparticles invariably end up in and around the normal cells, so that healthy tissue may be damaged when lasers go after cancers. Additionally, lasers that are normally used for heating the fire particles continuous beams of infrared light. It propagates both beyond the heat of cancer cells and in normal tissue. In cases where tumors develop and tissues around the civil state, such as nerve or artery walls, collateral damage to healthy tissue can be debilitating or dangerous.

In an effort to reduce the development of therapy, Lapotko and colleagues sought to change the approach to zapping nanoparticles. They started with mice that had been implanted with human squamous cell carcinoma, common cancerous cells in tumors and head of the human neck that are particularly difficult to treat with standard therapies. They have decorated their gold nanoparticles with proteins of immune antibodies that specifically lock on receptors which are seated on the surface of squamous cells. Which concentrates the particles, creating clusters of dozens of them in and around the cancer cells. And instead of pulling continuous laser beams, researchers fired only infrared ultrashort pulse.

As we expected, which prevented heat from spreading to surrounding normal tissues. But the approach has had an even more important effect: It caused temperatures to rise more where there were large clusters of gold nanoparticles. This vaporized adjacent water molecules, creating tiny bubbles that grow rapidly and burst, tear cancer cells. The key, Lapotko said, is that "nanoparticle clusters nanobubbles occur in cancer cells and not normal tissue."

online today Nature Nanotechnology , Lapotko and colleagues report that these mini explosions possible not only to retrieve sound where the tumor cells were located and thus detect the presence of only three cancer cells but it also destroys the cells in the process. in cases where it was possible to surgically resect most cancer tissues, 100% of animals survived, thanks to the fact that there is no residual tumor cells remained alive. And where the partial surgical removal of a tumor was an option, the survival rate for animals has doubled.

"This is very, very interesting," said Mien-Chie Hung of the University of Texas MD Anderson Cancer Center in Houston, which explores the treatment of tumors with nanoparticles. Hung noted that the approach fits very well with conventional surgery that is able to remove large tumors, but is unable to identify the cancer cells left behind. The new technique, he says, acts like microscopic surgery to target residual cells. Hung stressed that many approaches in oncology working in animals also found to be effective in humans. But if it does, it could open a new window in spots and the elimination of residual cancer cells left after surgery.

In an interview published in 1999, The Lancet , Scott Halstead said his biggest regret was not winning the Nobel prize, his worst habit cried a lot, and his favorite ways to relax was "skiing, tennis and sex (not necessarily in that order)." it was equally shameless of what he considered his greatest professional accomplishment :. affirming once controversial that antibodies against one type of dengue virus could "improve" subsequent infection by a different strain, leading to a fatal hemorrhagic fever

Halstead, now 86, is one world leaders on viruses spread by mosquitoes, including dengue, Japanese encephalitis and chikungunya. It continues to be a scientific provocateur, and he has interesting ideas about the probable fate of Zika and factors that may have converted from a human virus largely harmless in a major threat to infants.

Halstead began studying viruses transmitted by mosquitoes in 1957, when the US Army drafted him shortly after graduating from medical school. He remained with the army until 1965, running a virology laboratory in Thailand for 5 years. His long career then took him to Yale University, the University of Hawaii, the Rockefeller Foundation (he started the Children's Vaccine Initiative), Johns Hopkins University, and the Office of Naval Research. Since 1999, the base of the house was the Uniformed Services University of the Health Sciences in Bethesda, Maryland.

Science caught up with him on March 3rd for one night a phone call late while in Shanghai, China, in collaboration with a colleague there on dengue project

Q :. Early studies of Zika virus and yellow fever in populations of African apes found that viruses disappear for years, and then return. Last year you published an article on chikungunya which showed a similar act disappearance in human populations

A :. This virus was shown all over the world for centuries and every time it seems that everyone thinks it is a new event. When chik [ungunya] showed in Reunion [in 05], they thought it was the first time chik [ungunya] had never been that far from Africa. He did this every 50 years as long as the Europeans have sailed the Indian Ocean, and who knows what happened before. These things simply forgotten.

The Sultan of Zanzibar doctor makes these descriptions chik [ungunya] in 1870 and it looked like the virus appeared on the island of Zanzibar and then he crossed the Indian Ocean and created an epidemic across India. In his conversations with the elderly living in Zanzibar, he realized that the epidemic of 1823 had actually been around the Cape of Good Hope and went in the Caribbean.

People wonder how chikungunya escapes from East Africa and travel through the Indian Ocean, but the biggest mystery is why there is this periodicity of 50 years in Africa

Q: Do you think Zika have traveled around the same centuries ago unnoticed

a: No obvious. These Trans-Indian Ocean epidemics all seem to be chikungunya because of the deep arthritis that accompanies the disease. The latter Zika biological manifestation of passing the placenta and affect the fetus is absolutely new. If something like this happened in epidemic proportions, believe me, human beings have noted down

Q:.? What is the similarity between Zika, chikungunya and yellow fever that could explain this periodicity

A: The nature of these zoonotic diseases is that they involve primates. If you dug into it that you likely find it has something to do with time and fruiting trees and ape populations become really big and then you have the enormous animal diseases. There is no doubt that the herd immunity in humans must be very important, too, and the size of the population

Q :. Can you give an example

A: When I lived in Thailand in early 1960, we have intensively studied chikungunya and he was absolutely everywhere. By 1975, chikungunya had absolutely disappeared in Thailand.

Chikungunya had become endemic because Aedes aegypti population was extremely high and the human population was high. When I was in Thailand, the average household size was six. In the 1970s, family planning was introduced and within a generation the population of Thailand was reduced to two children per family today. Once you eliminate all those extra children in a family, you eliminate a huge percentage of the susceptible population that keeps the virus will.

We can actually measure the immunity of the herd and see when epidemics stop. The herd immunity [threshold] dengue for example, is about 80%. Chikungunya and Zika are probably the same, which means that when 80% of the population at risk is immune, the transmission is blocked four times out of five and one out of five is simply not enough to keep the current disease.

Q: Chikungunya first surface in the Caribbean in modern times in 2013. How long do you think that it will stay around

A: Five years, max. The only model I have is India. I was watching when chikungunya went from Africa to India in 1963 and disappeared from India in about 5 years

Q:.? Zika

A: Zika is the same

Q :. There is a great rush to make vaccines against Chikungunya and Zika because there is fear. But for Brazil, for example, when there is a vaccine, you suggest the country's population could be largely immune to Zika

A :. Exactly. It is like Ebola. It will be gone. We'll have that Ebola vaccine, which is about 85% done, and it will stay there until the next outbreak.

There are lots of people running around saying that he will be Zika and chikungunya in these new places forever. I do not think so. Based on the observations that I made and that everyone can see with their own eyes they look at the data, this virus is just going to get burned. There is only a need for a vaccine in the acute emergency

Q :. Do you think a enhancementlike antibody functionality with Zika is behind the serious illness that has been linked to microcephaly in babies and adults Guillain-Barré syndrome?

A: Absolutely. I am certain. I would bet a lot of money.

In the 1980s Ademola Fagbami Nigeria came to my laboratory at the University of Hawaii with Zika virus and we have experience, we published, which showed that it can be improved in mononuclear phagocytes [a type of immune cell]. We know that it thrives in these cells and the antibody can be improved. Zika is in fact genetically close enough to the dengue virus, which means a large number of zika on surface proteins are identical to the surface proteins of dengue. It absolutely would not surprise me to find that the antibodies of dengue infections and improve Zika that all this scanning Zika across the Pacific and South America have all been promoted and propelled by the development

Q :. What are the major unknowns about Zika

A: she -t grow in primary human monocytes in vitro? If someone dies can we find the virus in monocytes and macrophages in vivo? These are the key elements

Q:.? What could be the mechanism behind Zika harm fetus

A: I think the dengue antibody complexing with Zika virus and the immune complex is infected monocytes so you have a much higher amount of virus produced. Perhaps a certain concentration of virus, you start getting the virus spread in the placenta

Q :. When you suggested that antibodies against four different strains of dengue virus could improve was not immediately celebrated for the idea

A :. Let me tell you something, there's no fun to discover something that nobody wants to hear. I always thought to myself, I really discovered something very important, but in reality it is a bit horrible People make antibodies and kill. Nobody wanted to believe improvement dependent antibodies. The only problem is that it is true.

In response to political pressure and popular demand for a drug against cancer largely untested party, Brazilian President Dilma Rousseff signed into law today a measure that allows the compound to renegade phosphoethanolamine -Synthetic be produced and sold legally as a cancer therapy in Brazil.

scientists have poured scorn on the decision, saying it puts patients at risk and undermines the authority of the Brazilian Sanitary Surveillance Agency (the equivalent of the US Food and Drug administration) to regulate research and the approval of new drugs based on safety protocols and internationally recognized efficiency. It was a "political decision inspired by messianic thrust pseudoscience," said Gustavo Fernandes, president of the Brazilian Society of Clinical Oncology in Brasília. "This was the worst possible way to deal with this problem."

The "pill Cancer" sparked a national debate last year after Brazilian media carried stories of patients saying he relieved the symptoms or even cure their cancer. The compound was developed in the early 190s by Gilberto Chierice, an analytical chemist at the University of São Paulo whose lab distributed free to patients for several years without any regulatory approval or clinical monitoring.

apart some studies on mouse models and in cell lines, there is no laboratory evidence that synthetic phosphoethanolamine works as a medicine against cancer. The university tried to stop the operation of Chierice in June 2014, but since then more than 15,000 people sued the university, forcing him to continue to provide the pills. Advocacy groups, meanwhile, lobbied politicians and health authorities to legalize the use of the compound as a drug against cancer. Brazilian Congress passed a bill to do that last month.

Officials from the ministries of health, industry and the science advisable Rousseff to veto the bill, according to O Estado de S. Paulo newspaper. But Rousseff is fighting for his political life, Congress is trying to attack him on allegations of irregularities, its Executive Tax Office has recommended to sign the bill, according to sources.

The law permits the production, prescription and synthetic phosphoethanolamine consumption as a cancer therapy "independently" of the registration with the Brazilian Health Surveillance Agency. To acquire the pills, consumers must submit medical proof that they have a malignant tumor and sign a consent form.

Under the new law, the substance can not be produced and distributed by "licensed agents." On April 1st, the University of São Paulo closed the former research laboratory Chierice, which had hitherto been the production of pills under the orders of the court. The only place where the compound is being produced is a private laboratory contracted by the Government of the State of São Paulo to provide for an upcoming clinical trial. The laboratory prepares the pills according to a proprietary formula by Chierice and six colleagues; they affirm their preparation is different from the synthetic phosphoethanolamine available on the international market as a dietary supplement.

Late last year, the Ministry of Science committed to spending nearly $ 3 million on preclinical studies of synthetic phosphoethanolamine. The first results, released last month, are not promising. According to experiments conducted in four academic and private laboratories, the pills produced by Chierice group contained only 30% synthetic phosphoethanolamine, and the substance failed to kill cancer cells. It does not seem to be toxic.

At a hearing on April 5 at the Federal Senate of Brazil, Chierice charged that the government-sponsored studies are being "bad faith" and said his group is obtaining clinical data from 'overseas. The University of São Paulo in 2015 filed a complaint with the police accusing Chierice of " curandeirismo ," or the illegal distribution of unproven medical treatments. A criminal investigation is underway, according to reports press. "Maybe [Chierice] was well-intentioned, but he did a lot of harm," says Fernandes.

The new law may appeal to desperate cancer patients, but it is an unfortunate move, said biochemist Luiz Fernando Lima Reis, research director at the Sírio-Libanês hospital in São Paulo , where politicians have been treated for cancer, including Rousseff in 09 and former President Luiz Inácio Lula da Silva in 2011. "these types of decisions should be based on scientific evidence," said Reis.

Every time a celebrity dies in unclear circumstances, speculation in the wild. Most of the news reports about the rock star Prince died yesterday suggested the flu may have claimed his life. "Could Flu causing the death of Prince? Yes. Here's why," read a Forbes title. Other media used his surprising loss to 57 to remind readers of these flu risk and how it kills. TMZ, the celebrity gossip e-zine, "several sources" who say prince, despite being a Jehovah's Witness, received a "shot save" for a drug overdose six days before his death. The conspiracy-minded also came out of the woodwork and suggested that it was the vaccine against the flu, how his plane made an emergency landing, or yes, it is actually not dead at all .

Of course, it is possible that the prince died of the flu, and one of its representatives last week told reporters that a bad fight with the disease explained his emergency landing in Illinois and a hospital visit. Perhaps, as some reports have ventured there was a link between epilepsy and flu that ended his life. (A PubMed search for "flu, epilepsy, mortality" has a meager 23 results). But in the absence of new data, the data indicate that influenza is an unlikely explanation unless it had an underlying health problem, such as heart disease, which is known to increase the risk of death influenza. And of course, the surest way to find a probable rather than a possible answer to his cause of death is to conduct an autopsy, which is reportedly in progress.

According to the most authoritative study published by the US Centers for Disease Control and Prevention who analyzed the deaths of influenza in the United States 1976-07, support for over 65 suffers most high mortality by far, accounting for 87.9% of the deceased. (The study examines both flu and pneumonia deaths often related.) 19 to 64 age group was next at 10.6%.

A more granular study published by the American Lung Association found that mortality from influenza and pneumonia in 2013 was 8.3 per 100,000 people in the United States for 45-64 years and 107.4 per 100,000 for all 65 years old. From another angle, this year 6928 people in the 45 to 64 died from flu range. That's 81 million Americans in this age group. And keep in mind that many of those 6928 were of 57, which as you slice it, that means a few hundred people who were in their 57th year have died from the flu.

passing of Prince led BBC to go as far as making a history trend, "Why so many celebrities have died in 2016." a less satisfactory explanation: There are more famous than before. Or maybe there is more to rock stars of the baby boom generation ages simply.

flu, moreover, are not mentioned.

Vibrio cholerae , a bacterium comma-shaped contaminating water and food, can kill quickly. The acids in the stomach can erase billions of bacteria, but if a person swallows too little 1000 with food, some may survive the swim to the small intestine. There, the invaders will release enzymes to penetrate a thick layer of mucus that lines the epithelium. Once through, the bacteria will bind to epithelial cells and begin to divide, establish microcolonies that secrete toxins. Then the hour of death starts ticking.

Angered by the main cholera toxin, intestinal fluid gush, and a person will develop cramps, vomiting and, most notoriously, diarrhea that is fast becoming an impressive volume of "-water rice" plates: a aqueous liquid filled flakes mucosal and epithelial cells. In severe cases, people lose a liter of rice water stools per hour and without rehydration to replace the water lost from the body and electrolytes, may die in half a day.

The first question I ask is, "Do I want my children to participate ...?

In 1976, at the request of a panel of the US government, Myron "Mike" Levine 's University of Maryland School of Medicine in Baltimore began intentionally give humans V. cholerae . It is still today.

There are forty Levine was one of a small group of researchers doing studies supposedly human-intentionally challenge infect people with V. cholerae and other pathogens to test drugs and vaccines. But in recent decades, this practice, which has a long and checkered, "has become much more mainstream," says Levine. Stringent security procedures and new ways to reduce pathogens to reduce their risks lead investigators in the industry, universities and the government to take a new look at humans provocation tests, which provide a powerful tool for studying diseases and potential therapies. There is even a commercial enterprise, in hVIVO London, which specializes in human challenges. Today, people are deliberately infected with malaria, the flu, shigella, dengue fever, norovirus, tuberculosis, rhinovirus, Escherichia coli typhoid, giardia and campylobacter

the risks are obvious :. Otherwise healthy individuals may suffer damage and, if the disease is contagious, potentially sicken others. But if done well, the benefits are convincing a growing number of researchers say. The standard pharmaceutical development path for products that target pathogens slowly moves from the study of the security, administration, and biological responses in hundreds of people in a cost effective test with thousands of participants at high risk of being infected naturally. human challenge studies, which include a few dozen volunteers, accelerate the process of deciding to scrap or continue a promising, saving time and money. And tests that intentionally infect people can quickly and effectively flag potential side effects, lawyers say. "You can certainly make a $ 100 million study for each candidate vaccine seems safe and immunogenic," said Mark Mulligan, a molecular virologist who heads the vaccination center at Emory University in Atlanta and made human challenges with norovirus and tuberculosis.

Insights human challenges go well beyond drug and vaccine development. Christine Moe, another researcher from Emory University, has shown that the more easily transmitted norovirus via vomit diarrhea, and that "Ferrari viruses," famous for the speed at which it runs through vacationers on cruise ships, is impervious to alcohol based disinfectants and power wash oysters wear it. It notes that "sometimes human challenge studies are the only way to answer critical questions."

Checkered past

human challenges back to the 18th century and the first vaccine, when the English physician Edward Jenner tried to persuade the world that the infection of a person harmless cowpox could prevent the disease from its dreaded cousin smallpox. Jenner scratched the "material" taken from a cowpox sore on the hand of a dairymaid in the skin of 8 years old James Phipps, the son of his occasional gardener, then tried repeatedly to infect with smallpox. "Poor Phipps' as Jenner later called the boy never came down with smallpox. Jenner reported that some 6,000 people were vaccinated, then "well most of them" were challenged by smallpox. Two centuries later, the Jenner vaccine pioneer eradicated the virus in the human population.

intentionally infecting a single human leave a child with a disfiguring disease and even mortal would never pass muster today ethic. But as recently as the early 20th century, the intentional infection has been considered before -garde: Austrian psychiatrist Julius Wagner-Jauregg won the 1927 Nobel Prize in physiology or medicine for injecting the blood of people with malaria in patients with neurosyphilis, which the putative cured of madness and paralysis. As reporter Lawrence Altman documented in his book Who goes first? , many researchers have themselves questioned by pathogens to prove the value of their own experimental drugs or theories. Some died.

In the 1940s, the University of Chicago in Illinois and the US military have collaborated on provocation experiments that tested drugs against malaria in 400 Illinois prisoners. Nazi doctors, who horrified the world with their own medical experiments, including malaria tests that have killed hundreds of people, quoted American studies in their defense when they were tried in Nuremberg, Germany, in 1947. this led to the Nuremberg Code, which specifies what are now the standard search principles of informed consent, voluntary participation, and freedom to leave a review.

However, US experiments on prisoners continued, leading to 1973 presentation investigative journalist Jessica Mitford in The Atlantic Monthly, "experiences behind bars." Levine, who has just started his career, then the hard man with shigella and typhoid to the Maryland House of Correction in Jessup experiences, he insists were conducted ethically. "Studies in Jessup were two decades ahead of their time in terms of methods of informed consent," he said. But in 1976, the US National Commission for the Protection of Human Subjects of Biomedical and comportementale- the first attempt bioethics policy homeland issued a report that actually experiences of human provocation in prisons stopped.

outside prisons, however, research has continued. in 1974, the National Institute of allergy and infectious diseases (NIAID) in Bethesda, Maryland USA, has awarded the University of Maryland has half a million dollars to create a new vaccine testing center, led by Levine, who recruit volunteers and college religious groups. the center started with the challenges of the flu, which were conducted in the renovated rooms at the University of Maryland Hospital which had bunk beds for 22 people and an isolated air system. The researchers had little trouble recruiting volunteers, who received the same charges as jurors ($ 20 per day), the researchers considered only coercive but no. The volunteers had to pass a written test to prove they understand the risks.

Two years later, at the request of the Group of NIAID Cholera, Levine's group adds challenges V. cholerae to test cholera vaccines. "A very big questions was, 'Someone willing to participate?" Remembers Levine. "It is one thing to make the flu that most people live every two years or more, and it is another thing to take this exotic tropical infection and implement that."

Maryland required hospital fly a yellow flag to warn of quarantine cholera. Again, find volunteers presented some obstacles. "These are the same young people who were going down the hairy parts of the rivers on rafts," says Levine.

cholera studies led to the scuttling of a leading vaccine candidate, a more detailed understanding of effective immune responses, and, ultimately, convincing evidence that a vaccine against cholera different work. in June, the US Food and Drug Administration (FDA) will consider the approval of a vaccine against cholera for travelers based largely on the work of Levine. This is the most influential human challenge model has never played in the approval process of the FDA.

Modern volunteers

During the next decade, the Levine Group expanded with the challenges Salmonella typhi E. coli , and rotavirus. The only other important operation of human challenge was the common cold Unit established by the Medical Research Council in Salisbury, UK Then in 1985, a team led by Ripley Ballou began human challenges with malaria at Walter Institute Reed Army research (WRAIR) in silver Spring, Maryland. This pioneering program advances that have reduced the risk of human malaria problem and increased benefits, paving the way for successful tests today in several places.

Ballou, who now heads the R & D vaccine in the US to GlaxoSmithKline (GSK) and its high mosquito team in an insectarium, then have fed on human blood infected with the malaria parasite Plasmodium falciparum . He and five other colleagues from the army took each a candidate vaccine against malaria and let five infected mosquitoes, their group had determined was the number needed to transmit the parasite breakfast reliably on their arms then. "I am a full-fledged case of malaria and has never been sick in my life," says Ballou, although he was treated quickly. "It made a huge impression on me and I'm determined to find a way to stop this disease."

In the first WRAIR vaccine trial, all participants were "my friends in the laboratory or in the hallway," says Ballou, and they went home after being infected. Now WRAIR recruits special political-civilian governing the participation of persons serving in the army, which for a maximum of 10 days stay in a hotel together, where they receive regular checkups. Technology has also made safer experience when Ballou infected him Reaction test polymerase chain reaction can detect minute quantities of parasite DNA and identify infection two days earlier than the traditional microscope, and if volunteers receive immediate treatment, they rarely suffer symptoms [

impressive dividends challenge studies against the Army gave malaria. "We trashed a bunch of vaccines," said Ballou. They also contributed to the development of GSK RTS, S, the only vaccine against malaria, which has so far demonstrated its efficacy, albeit modest, in an essay on the large-scale field.

the resurgence

launched more recently trials face greater regulatory oversight as Levine and Ballou fact. Since the mid 190, the FDA found that the organisms used in the challenge studies are experimental drugs, and the agency has required researchers to submit new drug applications prior to testing. institutional review intensified, too .

human challenge studies with influenza provide an overview of the new landscape. in the 1980s and 190s, for example, Frederick Hayden of the University of Virginia School of Medicine in Charlottesville has conducted studies of provocation with the flu who have contributed to accelerate the development of Tamiflu and Relenza, drugs have become the mainstays of treatment. But the field work to a halt in 00 after a volunteer in one of the studies Hayden knew what the FDA calls an "adverse event". A 21-year-old man a heart defect testing drug against influenza developed after being questioned by the virus. "I still do not know what caused this incident," said Hayden. "There were a lot of sleepless nights." Mal Pas long occurred, but the incident has led to a thorough review of cardiac events in other influenza challenge studies.

So it was worrying when Matthew Memoli NIAID proposed new human challenge studies with the flu in 2011, which ultimately designed to test new treatments and vaccines . Some of his colleagues were so suspicious that the Department of ethics in the National Institutes of Health (NIH), the parent company of NIAID, was invited to conduct a formal review of the protocol. "We went through a lot 'steps, "said Memoli. Ethicists were particularly concerned about the proposed "high levels of payment" -up to $ 4000 but deemed this was not an "undue influence" because nobody was obliged to accept the offer.

the volunteers were "meticulously" projected, Memoli said. They had to be under 45 and undergo a battery of tests, including electrocardiograms Memoli and colleagues have also worked with the FDA to grow a strain of virus that has encountered good agency manufacturing practices, and they accurately calculated the minimum dose required to cause disease in most volunteers.

in ongoing studies, researchers spray the influenza virus in the nose of the volunteers through a fog, created by an atomizer that produces only particles larger than 10 microns. These relatively fat particles can cause infections of the upper respiratory tract, but do not reach the lungs, where the influenza virus can cause potentially fatal pneumonia. To avoid infecting others, participants remain in isolation rooms in the hospital for 9 days. "I challenged nearly 0 people and had no serious complications," said Memoli. "The worst thing that happened was a guy slipped in a shower."

Memoli notes that deliberately infecting people is a strange action for a doctor. "We deliberately make people sick," said Memoli . "It is a different idea of ​​what you are going behind to medical school. But over the next few years I think we will get information that will be extremely useful. "In a study published online in MBIO April 19, Memoli and colleagues reported that their challenge studies indicated that a response largely ignored the antibodies against the flu vaccines could be better predictor of the effectiveness of the antibodies analyzed regularly today.

Five years, the small community studying dengue began to discuss the provocation tests, which made people nervous, Durbin said Anna Johns Hopkins Bloomberg School of public Health in Baltimore infection mosquitoes can trigger high fever, severe joint pain, skin rashes and intense;. in rare cases, it can lead to bleeding and death. no drugs specifically target the dengue virus. "We hear, 'you can not treat dengue so you can not make a model of human challenge," said Durbin. human challenges with dengue date back a century, but the last intentional voluntary infections occurred in WRAIR in 01, and some of the participants developed dengue fever.

In 2011, WRAIR and NIH sponsored a workshop to discuss "reintroduction" model of human challenge for dengue. Several participants, including Durbin, argued that the tests could be carried out safely and would accelerate the development of a necessary evil for this disease vaccine.

With the blessing of the FDA in June 2013 Durbin began challenging volunteers who received vaccine against dengue is by NIAID. Instead of using the dengue virus from wild type Durbin Hopkins and his team infected with a naturally low virus isolate that was more attenuated in the laboratory. "I do not think you need to make people sick" to see if they develop an infection, said Durbin.

As she and her group reported online March 16 in Science Translational Medicine , none of the 21 people who received the vaccine infected after challenge, but every 20 checks the virus in their blood, and 16 developed a rash. Based in part on these results, the Butantan Institute in Sao Paulo, Brazil, this year launched a vaccine efficacy trial that plans to enroll 17,000 people.

Regulation of human challenge studies differ from one place to another. In the UK, for example, officers are questioning are not considered drugs, and experiences with them so do not require regulatory approval. A group at the University of Oxford led by pediatrician Andrew Pollard led a study of experimental vaccines against typhoid and paratyphoid challenge. Although both diseases are contagious, researchers allow volunteers to go home instead of staying in isolation. "They are potentially agencies that are in a relief flush toilet," says Levine, who works with the Oxford Group. "This is something that is not likely to be made in the United States."

The UK is "much more permissive," Pollard agrees, but says the tests pass by ethical depth reviews and the risk of transmission is "close to zero" if people have good hygiene.

the human challenge model has limitations, Levine points out, noting that his group refused to participate in an experiment carried out . Besides that put Neisseria gonorrhoeae in a penile catheter to study the transmission of gonorrhea "the first question I ask is:" Do I want my children, siblings, or spouse participate? "Said Levine. "If the answer is 'no', we do not do." And he fears that even if the address of the researchers of today risk more carefully than ever, someone might go too far and cancel the field gains made. "This should not be a Wild West show," he said. "Some newcomers may not be fully aware of the burden of the pioneers lived. It took a long time to obtain the support of everyone imaginable. "