"DESIGNER ESTROGEN" Scientists say an experimental hormone could be used to treat brain deterioration in a variety of conditions
CHICAGO The inkjet printer may appear to be an unlikely solution to organ-donor shortage, but it might not be as far-fetched as it sounds. Scientists have already used inkjet printers to "print" bacteria, yeast, and even human stem cells and they are exploring how to use the office workhorse to create 3D cell structures in a tissue matrix. If they can figure out how to create more complex tissues, they will be one step closer to creating implantable organs, a scientist said in a paper published in Science. "We've passed a milestone," said Paul Calvert, a material scientist at the University of Massachusetts in Dartmouth who has printed human stem cells. "We've shown that we can print cells and that they survive the process. If we can figure out how to build multiple layers of cells, then we're one step closer to creating an organ, and the ability to make functioning tissue-even in inelegant little lumps would still be useful." Teams of scientists in the United States, Britain, and Japan have been using modified inkjet printers to print cells for several years now-everything from single-cell organisms such as yeast to hamster ovary cells. They typically empty out the ink cartridges and fill them with solutions of cells, and reconfigure the appliance so that the nozzle spews the "bioink" on to some kind of growth medium rather than a sheet of paper. One of the chief advantages of the technology is that it's a convenient, noncontact way of depositing patterns of cells. Subsequent printing cycles don't disturb the material from previous cycles. Calvert and his team have already printed "human stem cells." Their challenge now is to construct simple layered structures to study the effect of proximity of different cell types on tissue development, using polymers or gels as scaffolds to separate and support the emerging tissues. "If we can grow two different cell types together, we can see how they communicate," said Calvert. The next step would be "to build complex three-dimensional tissues by printing the right precursors and enzymes in sequence. Given the right sources of the precursor proteins or compatible substitutes, we can build many passive structures such as bone, ligament, cartilage, and cornea," he wrote. The day when scientists can create life-size organs from scratch using inkjet printers is probably some way off. "I would be surprised if we could do it in 10 years. I would be disappointed if we couldn't do it in 30," said Calvert. But if scientists could create even a sliver of a liver or a heart this way in a laboratory, those tissues could be used for medical purposes, such as testing drugs, he noted.
CHICAGO Researchers have shown a designer estrogen can protect the brain against degeneration without increasing a woman's risk of breast or uterine cancer. They suggest that this "designer estrogen" could be used to treat brain deterioration in a variety of conditions including Alzheimer's disease, multiple sclerosis, Lou Gehrig's disease, spinal-cord injury, and even natural ageing. The experimental estrogen has only been tested on mice so far, but in those studies it halted the progress of the disease in mice infected with the animal version of multiple sclerosis (MS). The animals also recovered their ability to walk again. The hormone does not have antiinflammatory properties like regular estrogen because it has been adapted so that it does not express certain proteins that could cause cancer in women predisposed to malignancies of the breast or uterus. As a result, this form of estrogen would have to be combined with other treatments that combat the inflammation seen in MS and other illnesses, researchers said in their study published in the Proceedings of the National Academy of Sciences. "The main thing is to be neuroprotective. That's what's lacking in the field," said Seema Tiwari-Woodruff, an assistant professor of neurology at University of California Los Angeles David Geffen School of Medicine, who worked on the study. The findings offer potential for a "designer estrogen" that doctors could prescribe as part of an MS cocktail and also in higher doses without increasing a woman's cancer risk.
CHICAGO Scientists unveiled new research that could help doctors develop treatment preventing cells from dying when a patient suffers a heart attack or stroke. Much of the damage inflicted during traumatic injuries is in the form of cell death called necrosis, which was believed to be a chaotic, irreversible process. "For years, we believed that cell death related to a catastrophic insult such as a stroke or heart attack that deprives tissue of oxygen couldn't really be treated," said Gary Silverman, professor of cellular biology and physiology at Pittsburgh School of Medicine. "So we focused on strategies to prevent further damage by restoring blood flow as quickly as possible with clot-busters and surgery." But thanks to a series of experiments on worms, Silverman and his colleagues discovered that certain enzymes can kill a cell and possibly overwhelm its defenses following a stress or injury. The findings suggest that if scientists could find a way to enhance the production of natural inhibitors that combat these enzymes, they could prevent cells from dying. "Our research indicates that necrosis can be interrupted and possibly repaired, even after the injury process is well underway," he said of the study, which appears in Cell. The finding has far-reaching implications in the field of emergency medicine, and also in the treatment of the degenerative diseases such as Alzheimer's or Parkinson's, Silverman said.
TOKYO Japanese researchers say they have found a way to let people stroll through the virtual world of Second Life using their own imagination, in a development that could help paralysis patients. Previous studies have shown people can move computer cursors through brain waves, but the Japanese team says it is the first to apply the technology to an Internet virtual world. The technology "would enable people suffering paralysis to communicate with others or do business through chatting and shopping in a virtual world," said Junichi Ushiba, associate professor at Keio Univesity. Second Life is an increasingly popular virtual world in which people-and animals-are represented by animated avatars and can do everything from social activities to shopping. Ushiba said Second Life could motivate patients with severe paralysis, who are often too depressed to undergo rehabilitation. "If they can see with their own eyes their characters moving around, it could reinvigorate their brain activity and restore some functions," he said. Under the technology, a person wearing a head gear embedded with electrodes, which analyze brain waves in the cerebral motor cortex, would be able to move a Second Life character forward by thinking he or she is walking. Imagining movement with the right or left hand would make the character turn accordingly in the same direction. Researchers have previously put similar technology to work to scan brain waves to control objects such as computer cursors and electrical gears. In the Keio University laboratory, the team has designed artificial arms that operate by reading brain waves, although none is known to be commercially available yet. Ushiba said the technology could help people undergoing neurorehabilitation by stimulating brain activity. Traditionally, "if a stroke leaves a man's right hand paralyzed, he has been encouraged to use his left hand instead," Ushiba said. "More recently, however, it has come to light that the paralysed hand would start moving better if you try to use it," Ushiba said, noting that attempts to use a numb hand increase brain activity. The team next plans to test the technology on actual paralysis patients to see how they respond to the virtual world.
CHICAGO Scientists have known for decades that drastically reducing calories-but not nutrients-can prolong the lives of everything from yeast to mice and monkeys, but they didn't know why, until now. In a study published in Cell in September, US researchers suggest that the link between food restriction and longevity may be a molecular response to the stress from cutting back calories. That reaction preserves critical cellular functions, helping the body to fight off age-related diseases. In laboratory experiments on human cells, investigators found that cutting calories, while preserving the nutrients they need, starts a chain reaction in the mitochondria-power houses of the cell-that results in the buildup of a coenzyme called nicotinamide adenine dinucleotide (NAD). This in turn amps up the activity of enzymes created by two genes called SIRT3 and SIRT4. The effect of all this is to strengthen the mitochondria, increase energy output, and slow down the cell's ageing process. "We're not sure yet what particular mechanism is activated by these increased levels of NAD, and as a result SIRT3 and SIRT4," said David Sinclair, a molecular biologist at Harvard Medical School, who worked on the study. "But we do see that normal cell-suicide programs are noticeably attenuated," he said, referring to the way cells are programmed to die as part of the ageing and regeneration process. "This is the first time that SIRT3 and SIRT4 have been linked to cell survival." The fortification of the mitochondria in response to the stress of a much-lower-calorie diet can help ward off diseases associated with ageing. Damaged or dysfunctional mitochondria have been implicated in Alzheimer's, stroke, heart disease, and diabetes. It is thought that the common link is oxidative stress, which damages the mitochondrial DNA leading to cell death. Even given the growing recognition about the importance of the mitochondria in sustaining health, the researchers were surprised to find just how critical the so-called "battery packs" are to the life of the cell. Specifically, they found that even when all the other energy sources in the cell, including the nucleus, are wiped out, the cell remains alive if the mitochondria are kept intact and functional. "Mitochondria are guardians of cell survival," said Sinclair. "If we can keep boosting levels of NAD in the mitochondria, which in turn stimulates buckets of SIRT3 and SIRT4, then for a period of time the cell really needs nothing else." He added the genes could be promising drug targets for diseases associated with ageing. M |
