Health Meaning

criticism of fertilization potential in vitro (IVF) strategies to prevent babies from developing a common class of genetic diseases is sparking Controversy. In today's issue of Science three evolutionary biologists argue that ethical and scientific debate on an approach to experimental IVF called mitochondrial replacement minimized potential risks of the technique. While the trio further support the development of the therapy, they say that other animal studies may be needed before clinical trials should proceed. But supporters of the art and IVF key regulator in the UK say that the concerns have been addressed and are minor compared to the symptoms of technical prevent.

Mitochondria are organelles that provide cells with energy. The replacement of these power plants in egg cells has been proposed for women who carry mutations in their mitochondrial DNA (mtDNA), but still want to make a baby. (Mitochondria carry their own DNA, which is inherited almost exclusively by the mother, although spermatozoa mitochondria, they degrade after the fertilization of an egg.) Mutations in mitochondrial DNA can cause mitochondrial diseases, with an range of symptoms affecting the eyes, heart, brain and other organs. Some cases are mild; others are fatal.

The researchers worked to develop ways that women who carry mutations of mtDNA may have biological children without passing on the defect. Several methods are being developed, but they all involve replacing defective mitochondria from the egg of a patient with those of a healthy donor. The techniques raise ethical concerns because they involve changing the heritable DNA of an embryo "babies Three Mothers" is often part of the title that accompanies stories about the concept. In the UK, several ethical review committees scientific and technical gave cautious support, however, and the government has said it wants to allow the technique. It is planned to publish the proposed regulations in the coming months, and the UK Parliament could vote on a final version of the next year.

a number of animal studies have shown that the technique can produce live offspring, and a study last year showed that it can produce normal-looking human embryos, at least the blastocyst stage, about five days after fertilization. Some proponents of the technique compared to the evolution of the battery in a camera.

Klaus Reinhardt , an evolutionary ecologist at the University of Tübingen in Germany, and his co-authors say that this analogy is too simple. They say animal studies suggest that interactions between mtDNA and nuclear DNA are numerous, and minor changes in either can affect mitochondrial function. MtDNA donor presentation could lead to subtle problems in offspring that has not yet been studied in the only primate model for mitochondrial replacement: macaques. In mice and fruit flies, Reinhardt said, the problems of exchange mitochondria appear disproportionately in men and often affect fertility. macaques published studies on mitochondrial replacement follow the new offspring for 3 years, but men do not reach adulthood until 4 years, Reinhardt said.

The Human Fertilisation and Embryology Authority UK (HFEA), which would be in charge of regulating the technical if allowed in the UK, said his group of experts took these concerns into account. The panel "carefully examined the interaction between mitochondrial and nuclear DNA and concluded that the evidence did not demonstrate cause for concern," the agency said in a statement today. The agency talks with committee members to consider the question whether the monkeys in the study were followed long enough, a spokesman said.

geneticist Robin Lovell-development Badge of the MRC National Institute for Medical Research in London, who co-chaired the Scientific Review Committee HFEA, said he does not know of evidence that interactions between mitochondrial and nuclear DNA could cause serious health problems in humans. If treatment can lead to side effects, "it is important that the family knows that risk," he wrote to Science Insider in an email. However, he adds: "I think they would still choose [mitochondrial replacement] rather than having a sick child"

Reinhardt said he agrees. "We are sure HFEA. decide [whether to allow the therapy] based on a case by case basis and will be guaranteed. But couples who have mild mitochondrial disease may choose to wait two years until the monkeys are a little more mature. "

Bangkok- scientists have discovered a new type of virus that causes secular pestilence, dengue. The surprising discovery, announced at a major dengue conference here today, is bound to complicate efforts to develop a vaccine against the tropical disease becomes more widespread global threat. But it could shed light on where the pathogen came and if it is becoming a greater threat. The discovery "may change the way we think about dengue virus evolution and emergence," said Duane Gubler, a dengue expert at the Graduate Medical School Duke-NUS in Singapore.

This no vaccine or drug against dengue, which is transmitted by mosquitoes and causes fever and joint and muscle pain, sometimes excruciating pain. patients usually heal on their own, although cases serious need of medical support. sometimes, the disease progresses to the hemorrhagic dengue, a potentially fatal complication in which blood leaks through the vessel walls. a dengue infection confers lifelong immunity to this particular type. But subsequent infection with a second type increases the probability of a serious illness. in this spirit, vaccine developers have sought to protect against four types simultaneously.

this may have gotten more difficult. Fortunately, dengue virus samples screening researchers found a virus collected during an epidemic in the state of Sarawak in Malaysia in 07 they suspected was different from the original four serotypes. They sequenced the virus and found that it is phylogenetically distinct from the other four. Experiments have found that the monkey antibodies produced against the new type differ significantly from those arising from dengue virus already known. "We have discovered and characterized a new dengue serotype," said Nikos Vassilakis, a virologist at the University of Texas Medical Branch in Galveston, today at the Third International Conference on Dengue and dengue haemorrhagic fever.

"They did a great job in the characterization of the virus, and it is convincing that it is distinct from the other four," said Scott Thomas, an expert dengue at the University of California, Davis.

What this may mean for controlling dengue is uncertain. So far, dengue 5 was linked to a single epidemic in humans. Vasilakis suspect it circulates, perhaps among macaques in Sarawak forests. If it spreads, it could make the development more difficult human vaccines. "We do not need another complication in dengue control," says Scott.

Current efforts to control the disease are below. In the discussions here today, researchers from Malaysia, the Philippines and Thailand stated that despite the control programs initiated in the 00s, dengue cases are increasing, although the number of deaths is decreasing thanks to better management of severe cases. "dengue is spreading from urban to rural areas and countries, such as Nepal, where he has not been seen before, "said Samlee Plianbangchang, Regional Director World health Organization in South Asia. the global annual incidence near 30 million cases, is about three times the previously estimated load, the researchers reported in April in Nature .

despite a recent setback in the development of vaccines, Plianbangchang said that projects in the pipeline have researchers "forward to a vaccine in the near future." But he adds that a vaccine will complement, not replace, efforts to contain the dengue mosquito control and public awareness . "Dengue will be with us for many years and could get worse," he said.

Now there is a better way to spy the blood in your veins. Doctors already have two techniques to monitor obstructions in blood vessels, but both have limitations. The first, the ultrasonic Doppler imaging, involves irradiating tissue with ultrasonic waves; the waves that reflect off the blood flowing acquire a Doppler shift, which can be used to take blood and calculate its speed. Doppler can not distinguish the blood flow to surrounding tissue but unless it moves quickly, which makes the blood vessels invisible minors. The second technique, photoacoustic imaging, uses an infrared laser which, when absorbed into the blood, heats. The sudden expansion creates a resulting pressure wave that can be detected outside the body. photoacoustic imaging chooses the blood vessels better, but it can not see cast in a continuous stream. In a study published today in Physical Review Letters , the researchers combined both techniques, using the fact that ultrasound also has a slight warming effect; periodic pulsed ultrasound creates hot spots in blood vessels. By tracking the movement of these hot spots (in yellow above) using photoacoustic imaging, the team was able to calculate blood flow rates, even when he moved slowly through small vessels as capillaries. The researchers hope that their technique can help functional brain imaging, helping the detection of cancer and monitoring treatment, and that doctors detect atherosclerosis before a patient has a heart attack.

See Science Plans.

23andMe The company will no longer provide health information to people who buy his DNA test kit, it announced last night.The change was "to comply with the directive from the US Food and Drug administration to stop a new access to the consumption in our regulatory review process," the statement said. While current customers will always have access to 23andMe online database noting the health problems associated with their particular DNA, the company will not update this information, and customers who bought service staff genome ( PGS) or after November 22 will only receive information about their ancestry and their raw genetic data without interpretation.

The move comes after a letter of November 22 by the US Food and Drug Administration (FDA) warned the company, based in California Mountain View "to stop the marketing PGS immediately until it receives the authorization for the FDA to market the device. "the regulator has expressed various concerns, including that patients could change the dosage of medication or even abandon therapy because of the results of tests on 23andMe drug responses.

the action of the FDA has provoked a lively debate on the rights of people to learn their own genetic information and the authority of governments to regulate health-related marketing claims . 23andMe says on its website that its services are "for research, information, and the use of education only. We do not provide medical advice. "But the company focused on the medical uses of the test in the recent marketing, said Cecile Janssens, an epidemiologist at Emory University in Atlanta, who has studied risk predictions of accuracy led by 23andMe and others companies. " It used to be more about what science knows your DNA, "she said." But last year, they are really on another track. It is more about health recommendations now. "

A few days after the letter from the FDA, a complaint was also filed against 23andMe in a US District Court in California alleging that the test results provided by the company were" meaning " .

the European Commission needs to take an interest in the controversy over called gain function studies with dangerous viruses and should undertake a risk-benefit analysis for this line of research, 56 scientists from more than a dozen countries wrote in a letter to Commission President José Manuel Barroso. The letter accuses the December 18th European Society for Virology (ESV) making "misleading scientific claims" when he lobbied in support of Barroso studies hotly debated it 2 months ago.

concerned are studies to find out which mutations could be dangerous viruses such as the H5N1 strain of bird flu more easily transmissible between humans. Opponents of the research argue that its risks as an accidental leak of the laboratory, do not exceed the potential benefits.

ESV urged Barroso, who heads the executive arm of the European Union, to participate after Dutch court ruled that virologist Ron Fouchier of Erasmus MC in Rotterdam, the Netherlands, can not publish these studies with the H5N1 virus without first asking the Dutch government for authorization. (Fouchier appealed this decision .) In his letter of October 16 , ESV argued the decision could cause delays in the dissemination of scientific information and inequality between scientists from different European countries.

in their own letter to Barroso and several other members of the European Commission Fouchier critics charge there are "anomalies" in the ESV letter; for example, it is not true that research has been used only "to reproduce what nature already selected," the group wrote, because studies of Fouchier tours of virus never seen before. The group proposes to hold a scientific briefing of the Commission and calls on Barroso to organize a rigorous risk-benefit analysis of "decision-makers in Europe and the world."

Among the signatories, some ESV are members- are German virologist and Nobel prize Harald zur Hausen, Roel Coutinho, the former head of the infectious diseases control Centre in the Netherlands; and Adel Mahmoud, a former president of Merck Vaccines now in Princeton University.

Many people take vitamins such as A, E and C, thinking that their antioxidant properties will prevent cancer. But some clinical trials have suggested that these antioxidants, which sop molecules DNA damaging called free radicals, have the opposite effect and increase the risk of cancer in some people. Now, in a provocative study that raises disturbing questions about the widespread use of vitamin supplements, Swedish researchers have shown that relatively low doses of antioxidants stimulate the growth of early lung tumors in cancer-prone mice, perhaps by preventing suppressor gene known tumor.

For the complete story, see this week's issue of science .

honey bees are apparently Typhoid Marys of the world pollinator. One study suggests that bees spread two kinds of pathogens to wild bumblebees. And one of them, the virus deformed wing (DWV), kills bees across the UK may have contributed to the decline of wild populations of the nation. The high occurrence of DWV is "truly alarming", said Peter Neumann molecular ecologist at the University of Berne, who was not involved in the study.

DWV can be nasty. Like many other viruses in bees, DWV spreads in two ways. Honey worker bees ( Apis mellifera ) orally transmitted to other workers, usually causing a mild infection. But the parasite varroa is a support, too. When the mite feeds on bee pupae, infecting them with DWV, the virus causes horrific malformations. The young bees develop with swollen abdomens and shriveled or wrinkled wings, causing one of the worst DWV viral diseases in commercial bee hives

DWV first shot in 04 in commercial bumblebees. the insect Bombus terrestris , is often used in greenhouses, especially to pollinate tomatoes. Commercial breeders initially noticed that about 10% of bumble bees died tiny misshapen wings. Then Elke Genersch the Bee Research Institute Hohen Neuendorf, Germany, and his colleagues discovered that the dead bees were infected with DWV. The researchers suspected that the bees were orally infected bumblebees, because farmers use bees to encourage bumble bees to start new nests.

Nobody knew the extent of DWV in wild bumblebees. Matthias Fürst and Mark Brown of Royal Holloway, University of London, Egham and colleagues collected bees and bumblebees than 26 sites across Britain. The virus was present in 11% of bumblebees and replicate in more than a third of them, suggesting active infection, they report in Nature . The virus is probably more common than these data indicate, Brown noted in a telephone news conference. Bees "on their death bed, will not be taken by our sampling plan," he said

The team found genetic evidence that the virus is shared between species :. When bees and bumble bees lived near each other, the two had a similar strain of the virus. Because DWV was more common among bees, 36% were infected, researchers believe it propagates them to bumblebees. The team also found the same pattern with the fungal pathogen Nosema ceranae , but it does not cause problems for bumblebees.

DWV, secondly, spelled trouble. When researchers fed bumblebees food contaminated with the virus, the symptoms of the disease appeared. (See pictures of bumblebees with deformed wings, not of this study.) The worker bees became ill and died on average 6 days earlier than normal, a significant reduction of the typical life span of 21 days. A bumblebee nest contains less than several hundred worker bees, so any DWV generalized infection could devastate the nest capacity to collect enough food.

Jeff Pettis of the US Department of Agriculture Bee Research Laboratory in Beltsville, Maryland, agrees, it is likely that bees infect bumblebees. "This highlights the need to better manage bees in a responsible manner and to find ways to keep all pollinators," he said. Wild bumble bee populations, which help pollinate certain crops seem to decrease in many places, so the need is urgent. There is no way to treat sick bees, so the best strategy is to keep the honey as healthy beehives as possible, including controlling the varroa mite which aggravate infections in bees.

dark chocolate really has a good body, and scientists now have a better idea why. Gut bacteria break down the large compound in its key ingredient, cocoa powder, into smaller molecules that may inhibit harmful inflammation, the researchers reported today at the meeting of the American Chemical Society in Dallas, Texas. In laboratory experiments, scientists have processed cocoa with stomach and pancreatic enzymes and the sample washed to remove soluble molecules in water. They then fed the insoluble material remaining bacteria cultured from samples lab members stool (yes, they pooped in a cup for this study) and fermented in anaerobic conditions similar to those of the ileum and colon. The fermentation products acted as anti-inflammatory when applied to monolayers of the digestive tract that researchers were exposed to inflammatory stimuli. The results suggest that we can thank our intestinal bacteria to give dark chocolate its touted health benefits.

See Science Shots.

Get the vaccine against measles, and you will not be measles or give it to someone else. Right? Well, not always. A person fully vaccinated against measles contracted the disease and transmitted to others. The surprising case study contradicts received wisdom about the vaccine and suggests that a recent wave of measles outbreaks in developed countries could mean more illness, even among the vaccinated.

Regarding the vaccine against measles, two shots are better than one. Most people in the US are first vaccinated against the virus shortly after their first birthday and return to a booster as a toddler. Less than 1% of people who receive the two shots is contracting the potentially deadly skin and respiratory infections. And even if a fully vaccinated person becomes infected, a rare condition known as "vaccine failure" -They were not thought to be contagious.

This is why a theater employee of 22 years fully immunized in New York who developed measles in 2011 was released without hospitalization or quarantine. But as Typhoid Mary, this patient was found to be unintentionally contagious. Ultimately, it transmitted measles to four others, according to a recent report Clinical Infectious Diseases ensuing symptoms in the 88 persons with whom "Measles Mary" interacted while she was sick . Surprisingly, two secondary patients had been fully vaccinated. And while the other two had no record of receiving the vaccine, they both showed signs of prior exposure to measles which would have given immunity.

Further examination of blood samples taken during treatment revealed how the immune Mary measles broke down. As a first line of defense against measles and other microbes, humans rely on a natural spur of IgM antibodies. As a wooden shield, they offer some protection against microbial attacks, but are not impenetrable. The vaccine (or the measles) prompts the body to complete the primary buffer with a stronger armor IgG antibodies, some of which are able to neutralize the measles virus so can not enter cells or spread to other patients. This secondary immune response is presumed to last for decades.

By analyzing his blood, the researchers found that Mary measles IgM mounted a defense, as if she had never been vaccinated. His blood also contained a powerful arsenal of IgG antibodies, but a review revealed that none of these IgG antibodies were actually able to neutralize the measles virus. It seemed that his immunity given vaccine had decreased.

While officials of Public Health assumed that immunity against measles still hard, the case of Mary measles highlights the fact that "the actual length [of immunity] after infection or vaccination is not clear, "said Jennifer Rosen, who conducted the survey as director of epidemiology and surveillance at the New York City Office of immunization. The possibility of decreased immunity is particularly worrying that the virus surfaces in major US hubs such as Boston, Seattle, New York, and the Los Angeles area. Rosen does not believe this one case merit a change in the vaccination such strategy, give adults booster shots, but she said the more regular monitoring to assess the strength of measles immunity people is justified.

If it turns that vaccinated people lose their immunity as they age, which could expose them to measles outbreaks seeded by persons who are unvaccinated increasingly common in the United States and other developed countries. Even a vaccine failure rate of 3% to 5% could devastate a school with several thousand students, said Robert Jacobson, director of clinical research for a vaccine against the Mayo Clinic Research Group in Rochester, Minnesota, who was not involved in the study. Still, he said, "vaccine failure" The biggest thing with measles happens when people refuse the vaccine first. "

It's been 7 years that dozens of children with progeria, a devastating disease that causes symptoms resembling premature aging, began receiving an experimental drug called lonafarnib. That's an eternity for them and their parents as most afflicted with the extremely rare condition die in their teenage years. There is now a clue that this medical bet paid off, at least to a small extent. The Progeria Research Foundation (PRF), which funded the initial drug testing and ongoing monitoring and involving two other medicines, announced this week that interventions have probably added on average about 19 months for periods children's life.

This is "an important first step," said Leslie Gordon, a physician who, with her husband, founded PRF after their son was diagnosed with progeria. "Although these drugs are not curative, we show for the first time that life can be affected in children with progeria. "But this finding, detailed in a study published online may 2 in Traffic , has many scientists wondering if the results are significant, because the tests were missed an untreated control group as is sometimes the case for treatments for extremely rare diseases.

Only about one in 4 million to 8 million newborns have a mutation in a gene called LMNA causes what is officially known as progeria syndrome Hutchinson-Gilford. LMNA normally produces a protein that helps to provide a scaffold for the nucleus of a cell. The mutation leads to the accumulation of an abnormal version of the protein, causing deformed nuclei and other changes in the cells. The end result is a set of symptoms resembling premature aging of certain tissues: hair and weight loss, thin skin, joint stiffness, and atherosclerosis. This leads to heart attacks that cause the majority of deaths from the disease.

In 05, a study conducted by researchers at the University of California, Los Angeles, showed that a class of farnesyl transferase inhibitors drugs called (FTI), which block the binding of a molecule to defective protein allowing it to accumulate around the nucleus, restored normal form to kids with progeria cells. Several working groups with mice with the same mutation following established that the drug also reduces the signs of premature aging in rodents. Because FTI had already been tested in children with cancer without significant side effects, PRF quickly pushed to start a test of lonafarnib FTI in 07. Gordon, in collaboration with a team led by Mark Kieran oncologist Institute Dana-Farber Cancer Boston, initially followed 25 children as they received the drug for at least 2 years. The results of the test, published in 2012, showed that most patients had small gains and weight reductions in the stiffness of their blood vessels, although some scientists have found inconclusive and difficult to interpret.

In the new analysis, Gordon and his colleagues wanted to see if the children treated to date, including the first trial lonafarnib and those in an ongoing trial that adds two other drugs for the treatment survived more long as untreated children. But because there are so few children with progeria, and the disease is always fatal, PRF and designers in the study had agreed not to create a group receiving a placebo; all those who participated in the study received the drug, including the son of Gordon. For a comparison group, Gordon and colleagues instead of collecting data on untreated children from historical documents in the international register of the foundation, previously published case reports, and public databases.

This is what makes some question whether the extension of the apparent life is real. Studies with historical controls are "notoriously unreliable" said Donald Berry, a biostatistician at the University of Texas MD Anderson Cancer Center in Houston. Because various studies and databases can have an inclusion criteria patient, factors outside the drug's effectiveness could contribute to the life of differences. Gordon and his colleagues, however, have tried to solve this problem by matching children in the treatment group with untreated children the same age and sex, born after the subjects. the comparison showed that within 6 years after the start of treatment, those receiving the drug survived an average of 1.6 years longer than their untreated counterparts. in during this period, 21 of 43 children with progeria that has not included in the study died, against 5 of the 43 who had received treatment.

the discovery "is very rewarding and encouraging" said the doctor -geneticist Francis Collins, director of the National Institutes of Health in Bethesda, Maryland, whose research team studied the mechanisms and potential treatments for progeria. Collins acknowledges that the lack of direct control group enrolled in the trial is "not ideal", but noted "there was really not much of an alternative to what has been done, namely, to an open trial where all children had the chance to have access to the drug. "

But others, including Berry, are struggling to draw a positive conclusion from the study in the light of this limitation. It notes that a more dramatic improvement in life could overcome his doubts: "If patients have lived a normal life, then the results were convincing but even improved 'only' 10 years (and maybe even 5 years) would have been sufficient to establish the principle. which the treatment was effective. "

In addition to age and gender issues the Gordon team sent there differences between the countless trial participants and the untreated group, notes Howard Worman, a cell biologist and physician at Columbia University, who was the first to characterize LMNA gene. Children and their parents who enroll in a clinical trial may be more aware of their disease and more proactive with their health than non-participants, for example. "Until there is a matched group at the same time, ideally placebo-controlled, it is difficult to say whether there really is a survival advantage," he said.

Gordon and his colleagues are continuing to follow the children in the study who are still taking the IFT and the more time drug other two can make a clear survival advantage. His son, recently the subject of an award-winning documentary, died in January.