<img alt=“60773-haiti_300.jpg” src=“https://blogs.nature.com/nm/spoonful/60773-haiti_300.jpg” width=“300” height=“225” align=“right” hspace = “10 px”/>Last month, the United Nations released a long-awaited report indicating that human waste from Nepalese peacekeepers along with dirty drinking water likely triggered the spread of the cholera epidemic that has gripped Haiti since October, killing more than 5,000 people and sickening hundreds of thousands more.

The presence of foreign aid workers in the aftermath of last year’s earthquake, however, hasn’t been all bad. According to government officials, emergency response teams have helped contain the disease by providing clean water, medical treatment and sanitation systems. But with recent warnings that the numbers of people stricken with cholera could rise to 800,000 after the spring rainy season, global health experts say its time for a new approach to beat this infectious disease.

In a plan unveiled yesterday in PLoS Neglected Tropical Diseases, a team led by Paul Farmer, chief of the division of global health equity at Brigham and Women’s Hospital in Boston and a founder of Partners in Health, called for improved case detection, more aggressive treatment strategies and cleaner public water supplies to curb the spread of the disease.

“It’s important to recognize that we are losing the battle,” study co-author Edward Ryan, director of tropical medicine at the Massachusetts General Hospital in Boston, told Nature Medicine. “There has to be the use of new tools and old tools in new ways.”

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Since the early-1990s, scientists have known that farmers and other field workers are more likely to succumb to Parkinson’s disease because of their exposure to pesticides and other agricultural chemicals. But these studies fell short on showing a causal relationship between pesticides and the debilitating neurodegenerative disorder.

So, researchers turned to rodent models to prove the link. In the last decade, researchers found that three bug and weed killers promoted neurodegeneration in mice. And now, an independent team has validated those findings in a large epidemiological survey in humans.

The team led by Beate Ritz, an epidemiologist at the University of California–Los Angeles, estimated the average 25-year pesticide exposure for around 700 Californians, about half of whom developed Parkinson’s. Reporting in the European Journal of Epidemiology, the researchers found that people who lived or worked near farmlands treated with two commonly used agricultural fungicides — ziram and maneb — as well as the herbicide paraquat were three times more likely to develop Parkinson’s disease than those Parkinson’s disease than those were not exposed to these agricultural chemicals.

The results follow a previous study of residents from California’s Central Valley showing that people who lived near fields treated by two of these chemicals were 75% more likely to get Parkinson’s.

The findings “suggest that the critical window of exposure of toxicants may have occurred years before the onset of motor symptoms when the diagnosis of Parkinson’s disease is made,” Ritz said in a statement.

Looking ahead, Ritz and her colleagues urge lawmakers to establish monitoring programs to estimate pesticide exposure in rural communities in hopes of limiting people’s exposure to these agricultural chemicals and, ultimately, of getting Parkinson’s disease.

Image: Santiago Nicolau, Flickr Creative Commons

Heart disease is the leading cause of death in the United States, and costs the country upwards of $316 billion in terms of healthcare costs, drugs and lost productivity. Yet the methods currently used to identify those at highest risk of heart attack leave much to be desired. A team of researchers hopes to change that by introducing a new type of catheterization procedure that produces detailed images of the fatty buildup inside blood vessel walls in the heart.

“This may be a new way to identify high risk plaques in coronary arteries— the ones responsible for heart attacks,” says Farouc Jaffer of Massachusetts General Hospital in Boston, lead author of a paper describing the technology that appears in Science Translational Medicine today.

The approach uses an imaging agent known as near-infrared lipid-binding dye indocyanine green (ICG)—which is already approved by the US Food and Drug Administration (FDA)—to detect the fatty buildups likely to burst in the heart.

In this proof of principle study, the team fed one group of rabbits cholesterol-heavy foods for eight weeks, while keeping their control counterparts on a healthy diet. They then injected the dye, and 20 minutes later inserted a catheter, which as expected picked up more infrared signals in the rabbits on the cholesterol-rich diet.

In future, the Massachusetts General Hospital team plans to test this procedure in heart disease patients to determine its ability to identify those at highest risk of heart attack.

Image: Aorta after injection of ICG in an atherosclerotic rabbit. Courtesy of Science Translational Medicine/AAAS

Scientists are one step closer to understanding how cancer spreads thanks to a new technology based on real-time fluorescent imaging.

Reporting in Nature Materials yesterday, researchers describe how mechanical forces help coordinate cell movement and influence normal tissue growth. Their approach also sheds light on how cancerous cells break loose.

“What we think is happening in metastasis is that you lose this steering control and the cells break away and escape,” says co-leader of the study Jeffrey Fredberg of the Harvard School of Public Health in Boston.

Using a new technique dubbed ‘monolayer stress microscopy’, the team measured the forces between hundreds of cells in sheets of cultured healthy and cancerous breast tissue. The team found that cells form packs, which keep them in order. But the forces holding these cells together eroded in the tissue culture when scientists flooded it with proteins that promote growth*; ultimately this perturbation caused cells to break from the ranks and scatter in all directions. The scientists speculate that these rogue cells can then seed cancer in other organs in the body.

“We knew that these intercellular forces had to be important,” says Fredberg, “but we could never measure these forces until now.”

He hopes to use this method in the future to uncover how wounds heal.

To learn more about the emerging role of force in cancer metastasis, read our recent feature or check out our interactive slide show.

Image: A stress landscape. A map of the forces between cells in sheets of cultured rat lung endothelial tissue. Adapted from yesterday’s paper in Nature Materials.

*Updated 5/24/11: An earlier version of this sentence erroneously implied that the experiment observed the activation of oncogenes.

It’s official: Avandia will no longer be found on most US pharmacy shelves starting 18 November. After deciding last autumn to severely limit the use of GlaxoSmithKline’s beleaguered type 2 diabetes drug, the US Food and Drug Administration outlined new restrictions this week that will make the drug available only through a special mail-order program to diabetics whose blood sugar levels are not controlled by other drugs.

This decision follows a number of studies showing that Avandia (rosiglitazone) triggers more heart attacks than its competitor, Takeda’s Actos (pioglitazone). The European Medicines Agency suspended Avandia last year, forcing diabetics to find other medications to control their blood sugar levels.

“It’s like a decade-long nightmare coming to an end,” Steven Nissen, chief of cardiovascular medicine at the Cleveland Clinic, told USA Today. “Eleven years after this drug was introduced, it will be so restricted in access that virtually no one will be able to get it.”

Some people might be reluctant to give up Avandia, but, fortunately, alternative options abound. According to a meta-analysis out this week in the Annals of Internal Medicine, all other available diabetes drugs are just as effective when used to control blood sugar levels with two other conventional medicines. In the review of 18 clinical trials totaling around 4,500 participants, researchers from the Federal University of Rio Grande do Sul in Portugal found little difference in benefit between the thiazolidinediones (which include Avandia and Actos), alpha-glucosidase inhibitors (such as Bayer’s Precose), glucagon-like peptide-1 agonists (including Byetta’s Exenatide and Novo Nordisk’s Victoza) and dipeptidyl peptidase-4 inhibitors (which include Merck’s Januvia and Bristol-Myers Squibb’s Onglyza).

With an estimated 175,000 deaths attributed to hospital-acquired infections each year in Europe alone and a dwindling arsenal of effective antibiotics to combat these superbugs, researchers have been striving to develop new antibacterial medicines. But these efforts have been hampered by scientists’ limited understanding of the basic molecular machinery that microbes use to thwart medicine’s best weapons.

To gain a better picture of how pesky pathogens such as Escherichia coli generate defensive proteins, a team led by structural biologist Jamie Doudna Cate at the University of California-Berkeley turned to X-ray crystallography to obtain molecular snapshots of E. coli’s protein-producing ribosomes in action. Using these pictures, reported today in Science, Doudna Cate says researchers may be able to develop new antibiotics that stick a wrench in the ribosome’s works.

”There are a lot of great drugs out there but there are also bacteria becoming resistant to all of them,” Doudna Cate told Nature Medicine. “We need more targets.”

Image courtesy of Science/AAAS

Each year, an estimated 30,000 people in Africa are diagnosed with the crippling muscle wasting disease known as sleeping sickness. But the problem is far worse for the dairy and meat-producing cattle upon which their lives depend, as an estimated 5 billion cows die of Nagana, the animal form of the disease. Now, scientists hope to generate heartier, disease-resistant cattle — and the discovery of two new genes reported this week could help with that goal.

“The two genes discovered in this research could provide a way for cattle breeders to identify the animals that are best at resisting disease,” said Stephen Kemp, a geneticist at the UK’s University of Liverpool, in a statement.

In 1989, Kemp set out to eradicate the tsetse fly-borne disease in cattle with a simple strategy: his team crossed typical farming cattle called zebus to related disease-resistant West African cattle known locally as N’damas. Then, the researchers looked for traits that conferred sleeping sickness in resistant cattle. But the classical genetic methods his team used to find disease-resistant traits proved inconclusive. Kemp and his colleagues discovered 10 segments of the genome that conferred resistance, but the regions were simply too large and contained far too many genes to pinpoint the exact loci responsible for resistance.

With the help of functional genomics, however, Kemp’s team has now pinpointed two potential resistance genes in these regions. Using microarrays, the researchers identified a suite of genes that were switched on or off after infection in the heartier N’dama cattle. And after resequencing two genes of interest integral to fighting infections — ARHGAP15, which regulates neutrophil function, and TICAM1, which regulates dendritic cell migration — they identified disease-resistant alleles that had likely evolved in these West African cattle breeds to protect them from the disease.

N’damas themselves aren’t particularly good at plowing fields or producing milk. But by crossing these two resistant alleles from N’damas into zebus, researchers hope to create cattle breeds that are both resistant to disease and commercially productive.

Meanwhile, New York University biochemist Jayne Raper is taking a different approach to creating heartier cattle. As highlighted in our January 2011 news feature, Raper is hoping to take a resistance gene called APOL1 found in primates and into insert it into African cattle to make genetically-engineered, sleeping sickness-resistant cattle.

Kemp’s strategy might be more politically palatable, however. As Sue Welburn, a molecular epidemiologist from the UK’s University of Edinburgh who studies sleeping sickness in Uganda, told Nature Medicine in January: “People are reluctant to accept anything transgenic.”

Image: Stamp Out Sleeping Sickness Campaign.

By Mohammed Yahia

On 3 April, Qatar unveiled its first National Health Strategy (NHS), which covers the next five years and includes a plan to launch a new national governance body to better manage resources and projects across the various biomedical centers in the small Persian Gulf state. The newly proposed Qatar Medical Research Council (QMRC) will be based in Doha and will be responsible for coordinating research efforts between institutions and communicating the scientific outcomes to policymakers.

Currently, most of the scientific work taking place in Qatar is in basic biomedical research, and in 2006 the country committed to raising science funding to 2.8% of its gross domestic product. “Given the generous resources and the unwavering strive to excellence, it is worthwhile considering how to enhance the current elements involved in biomedical science and health research in Qatar,” says Momtaz Wassef, a former director of Qatar’s Department of Biomedical Research at the Supreme Council of Health who advised on the new NHS plan.

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