Researchers at Purdue University have built and demonstrated a prototype for a new class of miniature devices to study synthetic cell membranes in an effort to speed the discovery of new drugs for a variety of diseases, including cancer.

The researchers created a chip about one centimeter square that holds thousands of tiny vessels sitting on top of a material that contains numerous pores. This "nanoporous" material makes it possible to carry out reactions inside the vessels.

The goal is to produce "laboratories-on-a-chip" less than a half-inch square that might contain up to a million test chambers, or "reactors," each capable of screening an individual drug, said Gil Lee, the project's leader and an associate professor of chemical engineering.

For nearly a decade, scientists have been trying to fully understand a particular communication pathway inside of cells that contributes to many malignant brain and prostate cancers. While scientists have identified elements of this pathway, other key components have remained a mystery. Researchers at Whitehead Institute now have discovered a missing puzzle piece, a finding that may present drug makers with a significant new cancer target.

"We believe that we have identified a component that researchers have been looking for since 1996," says Whitehead Associate Member David Sabatini, who is also an Assistant Professor of Biology at MIT.

Tackling a pressing and controversial technical barrier in stem cell biology, scientists at the WiCell Research Institute and the University of Wisconsin-Madison have crafted a recipe that allows researchers to grow human embryonic stem cells in the absence of mouse-derived "feeder" cells, long thought to be a source of potential contamination for the therapeutically promising cells.

The new findings, appear today (Feb. 17) in the journal Nature Methods and come on the heels of a recent University of California study showing that existing stem cell lines are already contaminated with an animal molecule. The potential threat of animal pathogens tainting human stem cell lines poses a problem for the safe clinical use of many, if not all, of the current cell lines now in use.

Few events involving animals are more dramatic than when they band together and head out on the march cross-country. Among examples are the many thousands of wildebeests and other hoofed mammals that form herds and migrate across the African plains.

Countless millions of Mormon crickets and young locusts also sometimes unite with their own kind and form teeming, hungry islands of life that devour everything in their path that's edible. Some spectacular marching packs stretch several miles wide and extend 10 miles or so in length. And they can travel a mile or so a day.

Why such groups of insects form has mystified humans for thousands of years. One firmly held belief was that God was punishing men and women for their sins. A more recent, scientific theory has been the "safety-in-numbers" idea -- that the small animals congregate periodically as a way of protecting themselves from predators such as birds and rodents.

Now, a trio of insect experts has developed what they believe is strong new evidence that the latter theory is correct. By gluing radio transmitters -- each weighing less than half a gram -- to the backs of Mormon crickets in northeastern Utah and northwestern Colorado, Drs. Gregory A. Sword, Patrick D. Lorch and Darryl T. Gwynne showed experimentally that band formation indeed boosted insect survival.

New findings by researchers at UT Southwestern Medical Center challenge one of the established views of how nerve cells communicate with one another.

Every time we move, feel emotions, think or remember, the nerve cells, or neurons, in our body transmit messages to one another via chemical signals called neurotransmitters. Within neurons are tiny organelles called synaptic vesicles that sequester neurotransmitters and release them when needed into the synapse, or space between nerve cells, where the chemical signal is transmitted to other neurons.

It is known that synaptic vesicles release their neurotransmitters in two different "modes" – one when the neuron is stimulated and actively relaying a message, and the other through spontaneous release when the neuron is "at rest," or inactive. Until now it was believed that the same synaptic vesicles were responsible for releasing neurotransmitters in both modes.

However, new research by UT Southwestern scientists appearing in the Feb. 17 issue of the journal Neuron suggests that two distinct types of synaptic vesicles are responsible for the two different modes of neurotransmitter release – one type of vesicle for spontaneous release, another vesicle associated with activity-dependent release.