Web Concepts

Posts Tagged ‘health’

The women involved in the study used it only 60 percent of the time, and it was still effective -- meaning an even greater prevention rate is possible if it's used more frequently.

The study (PDF here) was published online Monday in Science.

The results still need to be confirmed, and scientists disagree about whether the protection it offers is sufficient to justify using the gel right away. But it's a major step in the fight to provide women another method besides condoms to protect themselves from infection. It's especially important in sub-Saharan Africa, where more than two-thirds of the world's HIV infections occur, according to AP.

Dr. Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases, tells AP the gel marks the first time researchers have seen any microbicide make a statistically significant impact.

The gel was announced at the International AIDS Conference in Vienna, where thousands of scientists, policymakers and activists are gathered. The next few days will include announcements about new drug therapies and genetic research, as well as discussions about funding for research and prevention.

The study involved 900 South African women who were administered a special gel spiked with the AIDS drug tenofovir. The gel cut the risk of HIV infection by 50 percent after one year of use and 39 percent after 2 1/2 years, compared to a gel that contained no medicine, according to the study. The women used the gel only 60 percent of the time, and those who used it more often had higher rates of protection. Scientists say more frequent use is key -- the gel does not need to be changed.

Of the 444 women who received a placebo gel, 60 became infected with HIV, versus 38 infections in the 445 women who received the microbicide, Science Express reports. That's a statistically significant difference, the researchers say.

The gel is in limited supply, but 99 percent of the women in the study said they'd definitely use it if they knew it prevented the spread of HIV.

[Science, RD Magazine]

The new bug is the first with complete resistance to the parasite -- and it passes that gene on to its children

For years, researchers have tried to engineer mosquitoes so that they're immune to the parasite that carries malaria -- a single-celled organism called Plasmodium. But previous attempts only succeeded in destroying about 97 percent of malaria parasites in mosquitoes' bodies. The difference between 97 and 100 percent might seem negligible, but Michael Riehle, who led the new study, says that 3 percent means the difference between success and failure. "If you want to effectively stop the spreading of the malaria parasite, you need mosquitoes that are no less than 100 percent resistant to it," he said.

In the new study, Riehle's team designed a piece of genetic information that inserts itself into a mosquito's genome. When the researchers fed malaria-infested blood to the modified mosquitoes, the Plasmodium parasites did not infect a single animal in the study. And once the anti-malaria molecule is injected into the mosquito's eggs, the next generation then carries the altered genes and passes it on to future generations.

The team also found that the anti-malaria molecule shortened the mosquito's lifespan, which minimizes chances that the malaria parasite will develop. Wild mosquitoes typically live for 2-3 weeks, but the malaria parasite needs 12-16 days to develop within the mosquito before it can be transmitted back to people. "The oldest mosquitoes are responsible for most malaria transmission, so reducing the lifespan of the mosquito can reduce or eliminate the number of people the mosquito can infect," said Riehle.

The malaria parasite is carried by the female Anopheles mosquito. When transmitted to a human, the parasite travels first to the liver and then on to the bloodstream, where it reproduces and destroys red blood cells. An estimated 250 million people contract malaria each year, and about 1 million die -- many of them children. There are currently no effective or approved malaria vaccines, although a few have been tested. Riehle says that even if a vaccine were developed, distribution would be a major challenge.

According to Riehle, completely eradicating the malaria parasite carried by mosquitoes requires three things: the ability to engineer the mosquito, finding genes or molecules that can kill the malaria parasite, and giving the modified mosquitoes a competitive advantage so they can replace the wild population. The first two components have been accomplished, but Riehle says the third represents a bigger hurdle. "A lot of research is being done now to give the mosquitoes fitness advantages so that they can replace the wild populations," he said. "But it's probably at least a decade away, and if this is ever used for malaria control it will take several years for population replacement to actually occur."

Riehle stressed that complete blockage of the malaria parasite is essential to any future control strategy -- if some of the parasites slip through the mechanism, then the next generation will likely be resistant to it. "If you release the mosquito and within two or three generations, it's no longer resistant to the malaria parasite, then you're back where you started," he said.

The genetically altered mosquitoes from the new study are being held in a secure lab environment that ensures they won't escape. Once researchers find a way to replace wild mosquito populations with lab-bred ones, the altered genes will hopefully spread through the natural population. If the approach ultimately succeeds, malaria could be a disease of the past.

The results of the new study were published today in the journal Public Library of Science Pathogens.

The vaccine is supposed to catalyze an immune response that strengthens the body against stronger strains of the pathogen. Generally that involves injecting a small dose of a pathogen into the vaccine recipient that provokes that immune response but, ideally, doesn’t make the person sick.

By turning to bacteria that live at the poles, the researchers were able to isolate certain genes that are responsible for essential processes like DNA repair or cell replication. However, in the polar bacteria these genes produce enzymes that only function at higher temps. Turn up the heat and the enzymes – and eventually the cells – die. By swapping these genes into pathogens, the team created strains that could live in cooler parts of the body to elicit an immune response, but would immediately die if they tried to move to warmer parts of the body like the vital organs.

To prove this, they took a human pathogen called Francisella novicida and swapped in some essential genes from its cold-weather counterpart Colwellia psychrerythraea. F. novicida can usually live in temperatures as warm as 113 degrees, but with its new genes it should perish at a more far less balmy 54 degrees. When injected into the relatively cold tails of lab rats, the F. novicida – which is deadly to mice – thrived locally but didn’t spread as it normally would. Moreover, when the rats were given a dose of normal F. novicida a few weeks later, the animals remained healthy.

Getting vaccines like this approved for distribution by regulators is no easy task because they are living things, but the U. of Victoria team hopes the method will lead to better vaccines to replace some current preventative treatments that are outdated, like that for tuberculosis. Such temperature sensitive strains could also simplify lab research on pathogens by creating strains of malicious organisms that are identical to their natural counterparts but for the fact that they can’t thrive within the human body.

[Science]

The MIT team, headed by professor of materials science and engineering Yoel Fink, has previously cobbled together heat sensitive and light sensitive materials, but adding piezoelectric functionality to these fibers adds a whole new dimension, giving materials the ability to convert mechanical changes in shape to electrical signals and vice versa.

But making these properties work together presents a particular challenge. In order to make their previous heat- and light-sensitive materials, Fink and company devised a method of layering the necessary materials into a thick "perform" cylinder that is then heated and stretched into a long, thin fiber. All these materials -- polymers, metals, etc. -- have to melt and stretch at similar temperatures. To make a piezoelectric layer, they had to do the same thing, mixing and matching polymers and polycarbonates to get a material that would heat and stretch uniformly and still retain its crystalline piezoelectric structures.

But after combining the earlier materials with the piezoelectric layer, the team now has a finished fiber that carries light as well as electricity. Vibrations or pressure generate an electrical signal, while electrical signals can be used to elicit mechanical changes in the fiber or cause vibrations that in turn can even be turned into acoustic waves.

Such materials could be used to perform a variety of tasks, not least of which is to monitor bodily functions via very tiny biosensors. The less-than-one-micrometer-wide fibers could be inserted into organs or the cardiovascular system to monitor for biomarkers or blood flow, while their ultrasound-like ability to perform acoustic sensing and carry infrared light essentially makes them tiny ultrasound imagers.

[Technology Review]

One of the antibodies suppresses 91 percent of HIV strains, more than any AIDS antibody ever discovered, according to a report on the findings published in the Wall Street Journal. The antibodies were discovered in the cells of a 60-year-old African-American gay man whose body produced them naturally. One antibody in particular is substantially different from its precursors, the Science study says.

The antibodies could be tried as a treatment for people already infected with HIV, the WSJ reports. At the very least, they might boost the efficacy of current antiretroviral drugs.

A vaccine for HIV, the virus that causes AIDS, would likely work by activating the body's own ability to produce antibodies that would ward off the disease. The latest discovery is more promising than a trial in Thailand last year in which scientists said an HIV vaccine reduced the chances of infection by just 30 percent. That study had also been plagued with controversy because in one analysis, the results were not statistically significant.

The WSJ says the new discovery -- involving scientists from the National Institutes of Health, Harvard Medical School, Howard Hughes Medical Institute and Columbia University -- is part of a renaissance in HIV vaccine research, which will be in focus later this month in Vienna, home to this year's International AIDS Conference.

It is welcome news for the the 33 million people the United Nations estimated were living with AIDS at the end of 2008.

The WSJ outlines the painstaking method the team used to find the antibody amid the cells of the African-American man, known as Donor 45. First they designed a probe that looks just like a spot on a particular molecule on the cells that HIV infects. Then they used the probe to attract only the antibodies that efficiently attack that spot. They screened 25 million of Donor 45's cells to find just 12 cells that produced the antibodies.

Scientists have already discovered plenty of antibodies that either don't work at all or only work on a couple HIV strains. Last year marked the first time that researchers found "broadly neutralizing antibodies," which knock out many HIV strains. But none of those antibodies neutralized more than about 40 percent of them, the WSJ says. The newest antibody, at 91 percent neutralization, is a marked improvement.

Still, more work needs to be done to ensure the antibodies would activate the immune system to produce natural defenses against AIDS, the study authors say. They suggest three test methods that blend the three new antibodies together -- in raw form to prevent transmission of the virus, such as from mother to child; in a microbicide gel that women or gay men could use before sex to prevent infection; or as a treatment for HIV/AIDS, combined with antiretroviral drugs.

If the scientists can find the right way to stimulate production of the antibodies, they think most people could produce them, the WSJ says.

[Wall Street Journal, Science]

Those effects are pretty serious; as the retina degenerates, the center part of a person's vision grows blurry or completely dark. The IMT corrects this by expanding an incoming image onto the peripheral parts of the retina that are still in good health. Once implanted directly into the cornea, the device makes use of the remaining working retina cells to produce a donut-like image that users can see.

Of course, that donut-like image isn't anything like our natural vision. Users have to go through a rehabilitation process to learn to see with their new eye, and even if a person has AMD in both eyes (most do) the IMT can only be implanted in one eye so the other can still provide peripheral vision. This kind of altered eyesight is likely headache-inducing, and may not work well for all candidates because of the intensity of the rehab process.

Further, the IMT is by no means a cure-all for all AMD. It is designed to treat a specific form of AMD known as "end-stage" (that's right, it's the more advanced stage of the condition), a kind of AMD that affects about 500,000 Americans. However, though far from a panacea, it is available right now and in two-thirds of trial cases the IMT has significantly improved vision, and by extension quality of life, in patients.

That's a pretty big deal, considering end-stage AMD is expected to affect more than a million patients by 2050. By then we'll all be cyborgs anyhow, but in the meantime the IMT should serve as a dependable technology that will keep more of the population in at least serviceable vision for longer.

[Singularity Hub]

The study authors defend their work, but said in a statement Wednesday afternoon that they were re-examining their analysis.

Specifically, Newsweek quotes an Icelandic geneticist who says the DNA analysis chip used for part of the study, the 610-Quad, has a quirk that can lead to false positives.

Kári Stefánsson, who founded deCode Genetics, says the quirk is related to two of the strongest genetic variants linked to aging in the study, called rs1036819 and rs1455311.

Newsweek reports: For any given gene, a person will have two alleles, or forms of DNA. In the vast majority of people, at the rs1036819 and rs1455311 locations in the genome, these pairs of alleles consist of one “minor” form and one “major” form. But the 610-Quad chip tends to see the wrong thing at those particular locations, according to Stefánsson.

The study in question found a pattern of genetic variants among people who lived to be 100 or older. The researchers, based at Boston University School of Medicine, built a model based on that genetic signature, and found it could predict longevity with 77 percent accuracy.

Scientists said the study, published in Science, was a breakthrough in understanding how genes affect human life spans.

But others immediately cried foul. Newsweek also quotes a Duke University geneticist, David Goldstein, who notes the researchers used different DNA chips to analyze the control group and the study group. The chips were manufactured by the same company, but they use different methods -- one studies 370,000 genetic variants and the other, the 610-Quad, studies 610,000 variants. The authors explain they had to change chips midstream because the 370 chip went off the market. Only about 10 percent of the people in the study were examined with the 610 chip.

Goldstein tells Nature.com that using different chips, or even the same chips in different labs, can influence the data. Some experiments turned up variants that seemed to be associated with a specific trait, but were actually due to slight differences in experimental conditions, he says.

Other concerns included the small sample size -- the BU team looked at 800 centenarians -- and the surprising accuracy of the model, at 77 percent.

The BU researchers stand by their findings, they said in a statement Wednesday afternoon: “We have been made aware that there is a technical error in the lab test used on approximately 10 percent of the centenarian sample that involved the two of the 150 variants. Our preliminary analysis of this issue suggests that the apparent error would not effect the overall accuracy of the model. Because the issue has been raised since the publication of the paper, we are now closely re-examining the analysis.”

They add that their statistical model holds up despite the small sample size.

Ultimately, further studies will be needed to clarify the findings. Some geneticists say they’re reserving judgment until the results are duplicated in a larger group of test subjects, such as a European group of 2,500 nonagenarian sibling pairs, according to Nature.

[Newsweek, Nature]