Boston Blog

Research Roundup: Measuring the weight of molecules and cells; working together to pinpoint diabetes genes; and how to spread rumors faster through a network

This week’s papers from Boston labs

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Nano-size scale weighs a single bacterium

MIT researchers have devised a miniature scale sensitive enough to weigh a single bacterial cell or even small clusters of proteins. The scale, which accurately detects the mass of particles at femtogram (10^-15^ gram) resolution, could eventually offer a rapid method for detecting pathogens or performing medical diagnostic procedures that involve counting cells.

Current nano-scales consist of a tiny, cantilevered platform that vibrates like a tuning fork. The presence of extra weight on the platform alters its vibration frequency, and the change is used to determine mass down to the zeptogram (10^-21^ gram) level.

But such detectors require a vacuum around the sample to be able to detect small changes in vibration. The presence of liquids, a critical requirement for the analysis of live cells or biological samples, interferes with the vibrations and vastly decreases the instruments’ capabilities.

To accommodate liquid samples, Scott Manalis of MIT and colleagues decided to put the sample inside the scale’s platform itself. They hollowed out a silicon chip with tiny channels, using it as the platform, and placed it in a vacuum. They were able to weigh the liquid samples as they flowed through the channels.

The researchers hope eventually to develop chips for rapidly and cheaply detecting bacteria, viruses, or toxins and counting human cells. For example, disposable chips could be used to count immune cells in the blood of AIDS patients. That could replace the expensive and bulky machines now needed to count cells and be a boon for poor countries where routine blood tests are impossible.

But getting to that point will require more work. Right now, the channels in the chips can accommodate bacteria, but not larger human cells. Future development will be aimed at enlarging the channels.

The work is published in this week’s Nature. Pat McCaffrey


Collaboration among competitors pays off for diabetes gene hunters

By cooperating rather than competing, three independent groups of scientists have jointly identified new genes that raise the risk of developing type 2 diabetes.

Local researchers from the Broad Institute headed up one of the groups, with help from collaborators at the Novartis Institutes for BioMedical Research in Cambridge, MA, and Lund University in Sweden. Their paper was published online yesterday in Science, along with others from U.S. and British research consortia.

The genome-wide hunt came up with three new diabetes-related genes and confirmed the involvement of several previously suspected ones. The work brings to 10 the number of genes or genomic regions linked to type 2 diabetes, a complex disease that is on the rise.

Previous studies suggested that many genes each contribute in a small way to diabetes risk. Sorting out the genetics required an exhaustive analysis—all told, the three studies involved 32,000 people from Britain and Scandinavia and examined millions of sequence differences in their DNA.

Unusually extensive data-swapping among the three independent groups allowed the researchers to rapidly confirm preliminary results and more confidently zoom in on interesting genes. Their example could serve as a model for research projects looking at other genetically complex diseases, such as heart disease and cancer.

Many of the newly discovered diabetes genes play a role in the development or function of the beta cells in the pancreas that produce insulin. Scientists now need to figure out the exact differences in the sequence of genes that contribute to the disease. The results may open up new avenues for risk assessment, diagnosis, and treatment of type 2 diabetes, a major contributor to the risk of heart attack, stroke, kidney failure, and blindness in industrialized countries. Pat McCaffrey


To spread gossip quickly, call your acquaintances, not just your friends

We are all part of networks of people and researchers are just beginning to understand how information spreads through these networks. It has a lot to do with our acquaintances, according to a new study of cell-phone calls. The weaker ties we have with people turn out to be crucial for the rapid transmission of information.

Albert-László Barabási at the Dana-Farber Cancer Institute and colleagues scoured the records of millions of cell-phone calls, determining the strength of ties between two people based on how much time they spent talking to each other.

The researchers built a model of this real-world, self-assembled network and then looked at how efficiently information flowed through the network if they severed certain ties but not others. They found that cutting the strongest ties among people had little effect on the ability of information to spread through the whole network. To their surprise, disrupting the weaker ties had more of an effect.

When they cut enough weak links, the network fragmented into many isolated groups—something that didn’t happen when they severed strong ties. This means, the researchers suggest, that sending information through the weaker links in the network could help it spread more quickly.

In this respect, the network of cell-phone conversations is unlike other well-studied networks, such as the Internet, which would be crippled if strong ties to key central hubs were disrupted.

So the next time you discover something juicy and want everyone to know about it, you may want to call up people you haven’t spoken to in years.

The work was published online this week in the Proceedings of the National Academy of Sciences. Mason Inman

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