.comment-link {margin-left:.6em;}

Forever in your prime

Anything I find interesting about how to slow, prevent, and reverse aging.

Tuesday, May 22, 2007

scientists develop tiny implantable biocomputers

 
CAMBRIDGE, Mass. -- Researchers at Harvard University and Princeton University have made a crucial step toward building biological computers, tiny implantable devices that can monitor the activities and characteristics of human cells. The information provided by these "molecular doctors," constructed entirely of DNA, RNA, and proteins, could eventually revolutionize medicine by directing therapies only to diseased cells or tissues.
 
The results will be published this week in the journal Nature Biotechnology.
 
"Each human cell already has all of the tools required to build these biocomputers on its own," says Harvard's Yaakov (Kobi) Benenson, a Bauer Fellow in the Faculty of Arts and Sciences' Center for Systems Biology. "All that must be provided is a genetic blueprint of the machine and our own biology will do the rest. Your cells will literally build these biocomputers for you."
 
Evaluating Boolean logic equations inside cells, these molecular automata will detect anything from the presence of a mutated gene to the activity of genes within the cell. The biocomputers' "input" is RNA, proteins, and chemicals found in the cytoplasm; "output" molecules indicating the presence of the telltale signals are easily discernable with basic laboratory equipment.
 
"Currently we have no tools for reading cellular signals," Benenson says. "These biocomputers can translate complex cellular signatures, such as activities of multiple genes, into a readily observed output. They can even be programmed to automatically translate that output into a concrete action, meaning they could either be used to label a cell for a clinician to treat or they could trigger therapeutic action themselves."
 
Benenson and his colleagues demonstrate in their Nature Biotechnology paper that biocomputers can work in human kidney cells in culture. Research into the system's ability to monitor and interact with intracellular cues such as mutations and abnormal gene levels is still in progress.
 
Benenson and colleagues including Ron Weiss, associate professor of electrical engineering at Princeton, have also developed a conceptual framework by which various phenotypes could be represented logically.
 
A biocomputer's calculations, while mathematically simple, could allow researchers to build biosensors or medicine delivery systems capable of singling out very specific types or groups of cells in the human body. Molecular automata could allow doctors to specifically target only cancerous or diseased cells via a sophisticated integration of intracellular disease signals, leaving healthy cells completely unaffected.

Monday, May 07, 2007

To Treat the Dead

The new science of resuscitation is changing the way doctors think about heart attacks�and death itself.
 
By Jerry Adler
Newsweek
 
May 7, 2007 issue - Consider someone who has just died of a heart attack. His organs are intact, he hasn't lost blood. All that's happened is his heart has stopped beating�the definition of "clinical death"�and his brain has shut down to conserve oxygen. But what has actually died?
Story continues below ↓advertisement
 
As recently as 1993, when Dr. Sherwin Nuland wrote the best seller "How We Die," the conventional answer was that it was his cells that had died. The patient couldn't be revived because the tissues of his brain and heart had suffered irreversible damage from lack of oxygen. This process was understood to begin after just four or five minutes. If the patient doesn't receive cardiopulmonary resuscitation within that time, and if his heart can't be restarted soon thereafter, he is unlikely to recover. That dogma went unquestioned until researchers actually looked at oxygen-starved heart cells under a microscope. What they saw amazed them, according to Dr. Lance Becker, an authority on emergency medicine at the University of Pennsylvania. "After one hour," he says, "we couldn't see evidence the cells had died. We thought we'd done something wrong." In fact, cells cut off from their blood supply died only hours later.
 
But if the cells are still alive, why can't doctors revive someone who has been dead for an hour? Because once the cells have been without oxygen for more than five minutes, they die when their oxygen supply is resumed. It was that "astounding" discovery, Becker says, that led him to his post as the director of Penn's Center for Resuscitation Science, a newly created research institute operating on one of medicine's newest frontiers: treating the dead.
 

A good night's sleep with the flip of a switch?

The flip of a switch could become all it takes to get a good night's sleep, according to a study released Monday. Researchers at the University of Wisconsin-Madison have found a way to stimulate the slow waves typical of deep sleep by sending a harmless magnetic signal through the skulls of sleeping volunteers.
 
Sleep remains one of the big mysteries in biology. All animals sleep, and people who are deprived of sleep suffer physically, emotionally and intellectually. But nobody knows how sleep restores the brain.
 
Now, Giulio Tononi, a professor of psychiatry at the University of Wisconsin-Madison School of Medicine and Public Health, has discovered how to stimulate brain waves that characterize the deepest stage of sleep. The discovery could open a new window into the role of sleep in keeping humans healthy, happy and able to learn. The study was published in the April 30 edition of the Proceedings of the National Academy of Sciences.
 
The brain function in question, called slow wave activity, is critical to the restoration of mood and the ability to learn, think and remember, Tononi says.
 
During slow wave activity, which occupies about 80 percent of sleeping hours, waves of electrical activity wash across the brain, roughly once a second, 1,000 times a night. In a paper being published this week in the Early Edition of the scientific journal PNAS, Tononi and colleagues, including Marcello Massimini, also of the UW-Madison School of Medicine and Public Health, described the use of transcranial magnetic stimulation (TMS) to initiate slow waves in sleeping volunteers. The researchers recorded brain electrical activity with an electroencephalograph (EEG).
 
A TMS instrument sends a harmless magnetic signal through the scalp and skull and into the brain, where it activates electrical impulses. In response to each burst of magnetism, the subjects' brains immediately produced slow waves typical of deep sleep, Tononi says. "With a single pulse, we were able to induce a wave that looks identical to the waves the brain makes normally during sleep."
 

Thursday, May 03, 2007

Breakthrough in regenerative medicine

Findings described in a new study by Stanford scientists may be the first step toward a major revolution in human regenerative medicine�a future where advanced organ damage can be repaired by the body itself. In the May 2007 issue of The FASEB Journal, researchers show that a human evolutionary ancestor, the sea squirt, can correct abnormalities over a series of generations, suggesting that a similar regenerative process might be possible in people.
 
Missing limbs, scarred hearts, broken spines, and wounded muscles always try to repair themselves, but often the result is invalidism or disease. Even some tumors try to revert to normal, but are unsuccessful. If the genetic sequence described in the sea squirt applies to humans, this study represents a major step for regenerative medicine.
 

Wednesday, May 02, 2007

Daily pill to beat genetic diseases

A pill that can correct a wide range of faulty genes which cause crippling illnesses should be available within three years, promising a revolution in the treatment of thousands of conditions.
 
The drug, known as PTC124, has already had encouraging results in patients with Duchenne muscular dystrophy and cystic fibrosis. The final phase of clinical trials is to begin this year, and it could be licensed as early as 2009.