Archive for March 2011
Posted March 27, 2011on:
Until now, there have been no witnesses to the death of brain cells in people with Parkinson’s disease.
And like any murder mystery, this has slowed the search for the killer.
In a big break in the case, Stanford University scientists say they have re-enacted this tragedy in a petri dish — growing the young neurons from the donated skin cells of Parkinson’s patient Genia Brin, the mother of Google co-founder Sergey Brin — and then watching them sicken and perish.
This feat, co-authored in this month’s issue of the journal Cell by Stanford’s Renee Reijo Pera, could accelerate the search for a cure of the crippling disorder. The research makes it possible, for the first time in medical history, to study the diseased cells and test compounds that might slow or even prevent their development.
“For the first time ever, we have them in a dish where we can study them directly. We can see exactly why they’re dying, and test drugs in them,” said Dr. William Langston of the Sunnyvale-based Parkinson’s Institute, who contributed to the effort.
Posted March 27, 2011on:
There are billions of neurons in the brain and at any given time tens of thousands of these neurons might be trying to send signals to one another. Much like a person trying to be heard by his friend across a crowded room, neurons must figure out the best way to get their message heard above the din.
Researchers from the Center for the Neural Basis of Cognition, a joint program between Carnegie Mellon University and the University of Pittsburgh, have found two ways that neurons accomplish this, establishing a fundamental mechanism by which neurons communicate. The findings have been published in an online early edition of Proceedings of the National Academy of Sciences (PNAS).
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Researchers have developed a way to create uniformly sized cell membranes, small cellular packages that can be used like tiny terrariums to study the inner workings of the cell and even create new molecules.
Sandro Matosevic and Brian Paegel of the Scripps Research Institute in Jupiter, Florida, have developed a chip-based method that creates uniformly sized vesicles in assembly-line fashion. Sized between 20 and 70 micrometers in diameter, the vesicles are large enough to be loaded with DNA and the biochemical machinery to act as synthetic cells. The synthetic packaging will help researchers study the proteins in cell membranes, which play important roles as gatekeepers of the cell. Many drugs, for example, act on these membrane proteins or otherwise use them to get inside cells in order to do their job.
Islands in the stream: Water droplets suspended in oil travel down a channel in a microfluidic chip. A stream of water flows alongside, forming an oil-water interface.
Credit: Brian Paegel lab, Scripps Institute
A sleepless night can make us cranky and moody. But a lesser known side effect of sleep deprivation is short-term euphoria, which can potentially lead to poor judgment and addictive behavior, according to new research from the University of California, Berkeley.
Researchers at UC Berkeley and Harvard Medical School studied the brains of healthy young adults and found that their pleasure circuitry got a big boost after a missed night’s sleep. But that same neural pathway that stimulates feelings of euphoria, reward and motivation after a sleepless night may also lead to risky behavior, their study suggests.
By mutating a single gene, researchers at MIT and Duke have produced mice with two of the most common traits of autism — compulsive, repetitive behavior and avoidance of social interaction.
They further showed that this gene, which is also implicated in many cases of human autism, appears to produce autistic behavior by interfering with communication between brain cells. The finding, reported in the March 20 online edition of Nature, could help researchers find new pathways for developing drugs to treat autism, says senior author Guoping Feng, professor of brain and cognitive sciences and member of the McGovern Institute for Brain Research at MIT.
A novel approach to pancreatic cancer treatment that activates the immune system works in some patients, according to a new study.
The treatment works by destroying the ”scaffolding” around cancer cells, says researcher Robert H. Vonderheide, MD, DPhil, an associate professor of medicine in the division of hematology/oncology and the Abramson Family Cancer Research Institute, University of Pennsylvania.
“The therapy is an antibody,” he says. ”Instead of binding to the cancer, this antibody binds to a molecule in the immune system, and that is CD40,” he tells WebMD. Next, the immune system is activated, allowing it to attack the so-called scaffolding around the cancer cells. The scaffolding is destroyed and the tumor falls apart.
The process is somewhat like attacking a brick wall by dissolving the mortar in the wall, he says.
By comparing the genome sequence of healthy and cancerous cells in 38 people diagnosed with multiple myeloma—an aggressive blood cancer—scientists have created a molecular map of what goes awry in this disease.
The findings, published today in Nature, point to new targets for drug development, and also suggest that some patients will respond to drugs currently being tested for other types of cancers.
The study is also the first published analysis of multiple whole genomes of the same cancer, reflecting continuing advances in sequencing technologies and the ability to analyze whole-genome data.