Treating HIV with an antibody can reduce the levels of the virus in people's bodies — at least temporarily, scientists report on 8 April in Nature1. The approach, called passive immunization, involves infusing antibodies into a person's blood. Several trials are under way in humans, and researchers hope that the approach could help to prevent, treat or even cure HIV. The work is a milestone towards those goals, says Anthony Fauci, director of the US National Institute of Allergy and Infectious Diseases in Bethesda, Maryland. “This is an early study, but it’s a study with some impressive results,” he says.
Researchers tested four different doses of an HIV antibody called 3BNC117 in 29 people in the United States and Germany. Seventeen of the participants had HIV, and 15 of those were not taking antiretroviral (ARV) drugs at the time of the study. One infusion of the highest dose of antibody, given to 8 participants, cut the amount of virus in their blood by between 8 and 250 times for 28 days.
But much work remains to determine whether the approach can produce longer-lasting effects and whether it is practical for clinical use. Previous studies have shown that passive immunization can reduce levels of HIV in the blood of monkeys and mice, although the approach has not worked as well in humans2.
But the antibodies used in those earlier clinical tests were of an older generation that could not neutralize many different strains of HIV. Researchers have spent much of the past decade trying to find 'broadly neutralizing' antibodies that are more widely effective against the virus, and the 3BNC117 antibody belongs to this class.
The price of treatment with this approach is also a concern. Antibodies can cost thousands of dollars for each course of treatment, and the majority of people with HIV are in low- and middle-income countries, some of which are already fighting drug companies over the high cost of antibody medicines. “The practicality, utility and efficacy of this approach are hugely open questions,” says Mitchell Warren, executive director of AVAC, a global organization that advocates HIV prevention and is headquartered in New York City.
Scientists seeking a cure for Aids say they have been inspired, not crushed, by a major setback in which two HIV-positive patients believed to have been cured found the virus reinvading their bodies once more.
New HIV infections among adults and children were estimated at 2.3 million in 2012, a 33% reduction since 2001. New HIV infections among children have been reduced to 260 000 in 2012, a reduction of 52% since 2001.
There could be hope for diabetics who are tired of giving themselves insulin injections on a daily basis. Researchers at North Carolina State University and the University of North Carolina at Chapel Hill are developing a system in which a single injection of nanoparticles could deliver insulin internally for days at a time – with a little help from pulses of ultrasound.
The biocompatible and biodegradable nanoparticles are made of poly(lactic-co-glycolic acid), and contain a payload of insulin. Each particle has either a positively-charged chitosan coating, or a negatively-charged alginate coating. When the two types of particles are mixed together, these oppositely-charged coatings cause them to be drawn to each other by electrostatic force.
One hundred sixty years after the invention of the needle and syringe, we're still using them to deliver vaccines; it's time to evolve. Biomedical engineer Mark Kendall demos the Nanopatch, a one-centimeter-by-one-centimeter square vaccine that can be applied painlessly to the skin. He shows how this tiny piece of silicon can overcome four major shortcomings of the modern needle and syringe, at a fraction of the cost.
Leeches are quite effective and approved by the FDA for circulation problems. ... How is it science is inconclusive as to why Building 7 fell but you state w/absolute certainty that injecting a newborn w/ heroic doses of mercury is all good.
Africa: Hashtags for Health AllAfrica.com ... insights into global and regional trends. Today, researchers are digging into Twitter, looking at what users are saying about disease in order to monitor epidemics.
New research indicates that senescent cells, those that stop dividing, play an important role at both the dawn and dusk of life.
In 1961, two biologists named Leonard Hayflick and Paul Moorehead discovered that old age is built into our cells. At the time, many scientists believed that if healthy human cells were put in a flask with a steady supply of nutrients, they would multiply forever. But when Dr. Hayflick and Dr. Moorehead reared fetal human cells, that’s not what they found. Time and again, their cells would divide about 50 times and then simply stop.
In fact, it turned out, senescent cells are involved in many of the ravages of old age. Wrinkled skin, cataracts and arthritic joints are rife with senescent cells. When researchers rid mice of senescent cells, the animals become rejuvenated.
Given all this research, the last place you would expect to find senescent cells would be at the very start of life. But now three teams of scientists are reporting doing just that. For the first time, they have found senescent cells in embryos, and they have offered evidence that senescence is crucial to proper development.
The discoveries raise the prospect that the dawn and dusk of life are intimately connected. For life to get off to the right start, in other words, youth needs a splash of old age.
Scott Lowe, an expert on senescence at Memorial Sloan-Kettering Cancer Center who was not involved in the research, praised the studies for pointing to an unexpected role for senescence. He predicted they would provoke a spirited debate among developmental biologists who study how embryos form. “They’re going to really love it or really hate it,” Dr. Lowe said.
While senescence may be a powerful defense against cancer, however, it comes at a steep cost. Even as we escape cancer, we accumulate a growing supply of senescent cells. The chronic inflammation they trigger can damage surrounding tissue and harm our health.
In the mid-2000s, William Keyes, a biologist then at Cold Spring Harbor Laboratory on Long Island, was studying how senescence leads to aging with experiments on mice. By shutting down a gene called P63, he could accelerate the rate at which the mice accumulated senescent cells — and accelerate their aging.
To observe the senescent cells, Dr. Keyes added a special stain to the bodies of these mice. To see the difference between these mice and normal ones, Dr. Keyes added the same stain to normal mouse embryos.
Naturally, he expected that none of the cells in the normal mouse embryos would turn dark. After all, senescent cells had been found only in old or damaged tissues. Much to his surprise, however, Dr. Keyes found patches of senescent cells in the normal mouse embryos. Dr. Keyes decided to look again at those peculiar senescent cells in normal embryos. He and his colleaguesconfirmed that cells became senescent in many parts of an embryo, such as along the developing tips of the legs.
The researchers, however, found no evidence that the senescent cells in embryos have damaged DNA. That discovery raises the question of how the cells were triggered to become senescent. Dr. Keyes hypothesizes they did so in response to a signal from neighboring cells.
Once an embryonic cell becomes senescent, it does the two things that all senescent cells do: it stops dividing and it releases a special cocktail.
The new experiments suggest that this cocktail plays a different role in the embryo than in the adult body. It may act as a signal to other cells to become different tissues. It may also tell those tissues to grow at different rates into different shapes.
Dr. Keyes suspects that the sculpting that senescent cells carry out may be crucial to the proper development of an embryo. Consequently, any disruption to senescent cells may have dire consequences. “Where we see senescence in the embryo is where we see a lot of different birth defects,” he said.
For an embryo to develop properly, signals have to be sent to the right places at the right times. The peculiar behavior of senescent cells may help in both regards. If a cell stops growing, it won’t spread too far from a particular spot in an embryo. And by summoning immune cells to kill it, a senescent cell may ensure that its signals don’t last too long.
It’s possible, Dr. Keyes speculates, that senescence actually evolved first as a way to shape embryos; only later in evolution did it take on a new role, as a weapon against cancer. “I like the idea that it was a simple process that was then modified,” Dr. Keyes said.
One in eight people around the world is chronically undernourished, the United Nations' food agencies said on Tuesday, warning world leaders that some regions would fail in halving the number of hungry by 2015.
Sharing your scoops to your social media accounts is a must to distribute your curated content. Not only will it drive traffic and leads through your content, but it will help show your expertise with your followers.
How to integrate my topics' content to my website?
Integrating your curated content to your website or blog will allow you to increase your website visitors’ engagement, boost SEO and acquire new visitors. By redirecting your social media traffic to your website, Scoop.it will also help you generate more qualified traffic and leads from your curation work.
Distributing your curated content through a newsletter is a great way to nurture and engage your email subscribers will developing your traffic and visibility.
Creating engaging newsletters with your curated content is really easy.