Syndicate content

Archive - Jun 15, 2009

Electronic Nose May Sniff Out Early Kidney Disease

Scientists may have discovered an ingenious way to detect chronic renal failure (CRF) at its earliest and most treatable stages. The method would involve the electronic detection of volatile molecules found in the breath of those with developing kidney disease, but not in the breath of those without kidney disease. The promise of this approach was supported by experiments in rats where an “electronic nose” was used to detect 27 volatile organic compounds that appear in the breath of rats with no kidney function, but not in the breath of rats with normal kidney function. The “electronic nose” is based on a technology in which a semi-conductive random network of single-walled carbon nanotubes and insulating nonpolymeric organic materials provides arrays of chemically sensitive resistive vapor detectors. The results presented in this study raise expectations for future capabilities for diagnosis, detection, and screening various stages of kidney disease, the researchers said, noting that the tests could detect patients with early disease, when it is possible to control blood pressure and protein intake to slow disease progression. The researchers pointed out that the blood and urine tests now used to diagnose CRF can be inaccurate and may come out "normal" even when patients have lost 75 percent of their kidney function. The most reliable test, a kidney biopsy, is invasive and may result in infections and bleeding. Doctors have long hoped for better tests for early detection of kidney disease. The current research was reported in the May 26 issue of the American Chemical Society journal ACS Nano. [ACS Nano abstract]

Microchannel Device Could Trap Cancer Cells

Scientists at Northwestern University have developed a novel method that can be used to separate metastatic cancer cells from normal cells. They have proposed that the method could be used to create a “cancer trap” using implantable and biodegradable materials. A device they have currently developed illustrates the method. The device takes advantage of a physical principle called ratcheting and is a very tiny system of microfluidic channels for cell locomotion. Each channel is less than a tenth of a millimeter wide. Asymmetric obstacles inside these channels direct cell movement along a preferred direction. To sort metastatic cancer cells from normal cells, the scientists took advantage of the cells' different shapes and mobility characteristics. Migrating cancer cells tend to be rounder and broader, while normal epithelial cells are long and thin with long protrusions on the ends. The researchers designed a channel with "spikes" (rachets) coming out at 45-degree angles from the walls, alternating on opposite sides of the channel. This pattern funnels cancer cells in one direction, while at the same time directing normal cells in the opposite direction. The researchers showed that a device with a number of these channels leading to a central reservoir, like spokes on a wheel, worked just as well at separating cancer and non-cancerous cells. A stack of these radially arranged ratchet channels could be used to create a "cancer trap," the researches suggested. "When implanted next to a tumor, the particles [stack of rachet channels] would guide cancer cells, but not normal cells, inward to the reservoir, where they would be trapped," said Dr. Bartosz Grzybowski, the paper's senior author.

Huntington Disease Clue Discovered

Researchers have demonstrated that mutated huntingtin protein, but not normal huntingtin, activates a neuron-specific protein (JNK3) which inhibits fast axonal transport, a system used to shuttle proteins from the nerve cell body, where they are made, to the synaptic terminals, where they are needed. This discovery might help explain the curious nervous system specificity of Huntington disease, even though the huntingtin protein is expressed in other parts of the body. "Inhibition of neuronal transport is enough to explain what is happening in Huntington's," asserted Dr. Scott Brady, senior author of the report. Loss of delivery of materials to the synaptic terminals results in loss of transmission of signals from the neuron. Loss of signal transmission causes the neurons to begin to die back, leading to reduced transmissions, more dying back, and eventual neuronal cell death. This mechanism might also explain the late onset of the disease, Dr. Brady said. Activation of JNK3 reduces transport, but does not eliminate it. Young neurons have a robust transport system, but transport gradually declines with age. "If you take a hit when you're very young, you still are making more and transporting more proteins in each neuron than you need," Dr. Brady said. "But as you get older and older, the neuron produces and transports less. Each hit diminishes the system further. Eventually, the neuron falls below the threshold needed to maintain cell health." This work was reported online on June 14 in Nature Neuroscience. [Press release] [Nature Neuroscience article]