HEARING SECRET
Researchers unveil the mechanisms that switch on the ability to hear
Molecule reverses symptom of muscular dystrophy
WASHINGTON
Researchers have created a synthetic molecule that reversed a key symptom of muscular dystrophy in mice, raising hope in the battle against the debilitating disease. The University of Rochester Medical Center researchers injected a component into mice that eliminated myotonia, a symptom which in people causes muscles to tense up and weaken, the study said.
"The significance of this work is the proof of concept that a fundamental aspect of this genetic disease can be reversed even after it is very well established," said Charles Thornton, codirector of the university's Neuromuscular Disease Center. "It encourages us to believe that other parts of the disease could be reversible as well," said Thornton, the senior author of the study published in the Journal of Clinical Investigation.
But the researchers warned that more work was needed before the molecule could be tested on humans. The synthetic compound, known as a morpholino, that was injected in the mice's muscle cells revived their chloride channel, a crucial cellular mechanism that controls electrical activity in muscles, the study said. After the mice were injected with the compound, which the university team designed with the biotechnology company Gene Tools, the symptoms all but disappeared and did not return for several weeks.
The chloride channel is essentially disabled in humans with the disease, making it difficult for a person to relax the muscles. For instance, a person suffering from myotonic dystrophy may be unable to release an object after grasping it.
Revealed: The superbug's superbug
PARIS
Scientists believe they have explained how a highly virulent strain of the superbug called methicillin-resistant Staphylococcus aureus (MRSA) is able to dodge the immune system. This strain, called community-acquired MRSA, or CA-MRSA, is more vicious than the hospital-borne strain of MRSA, the trigger for a global scare surrounding bacteria that are impervious to all but a handful of antibiotics.
CA-MRSA causes severe skin infections, including "flesh-eating" necrotising fasciitis, and potentially fatal blood poisoning. It is now the cause of the most infections that result in trips to the emergency room in US hospitals, the New England Journal of Medicine reported last year.
Investigators led by Michael Otto of the National Institute of Allergy and Infectious Diseases found that CA-MRSA strains secrete a much higher level of small peptides or protein fragments called phenol soluble modulins. They believe these peptides play a stealthy but important role in helping the bacteria to cause disease by worsening inflammation and killing red blood cells and neutrophils. They tested their hypothesis on mice. Bacteria that had been genetically manipulated to lack phenol-soluble modulins had a far less virulent effect on the rodents.
The study is published in Nature Medicine.
Turning on the sound
PARIS
A study published in Nature has uncovered mechanisms that switch on the ability to hear. Cells located in a auditory structure called Koelliker's organ release a rush of adenosine triphosphate (ATP), a molecule that shuttles energy around to other cells. The burst of ATP stimulates nearby inner hair cells-the cells that respond to sound waves-into releasing an amino acid called glutamate. This in turn activates primary auditory neurons, the nerve fibers that send an electrical signal to the brain when a sound is detected.
The study, led by Dwight Bergles of Johns Hopkins University in Baltimore, Maryland, was carried out on newborn rats, which cannot hear airborne sounds until their middle and inner ears mature. Researchers hope the findings could be useful in understanding tinnitus, the "ringing" in the ears that occurs even though there is no sound.
Pioneering surgery saves baby in womb
BERLIN
A German hospital is celebrating a world first after carrying out life-saving surgery that stimulated lung growth in a baby still in the womb. Doctors at Bonn University Clinic feared that the baby would die when her mother's fetal membrane burst in the 20th week of pregnancy, removing the child's protective liquid cushion. Without the fluid, the organs pressed on the lung and the baby's development was being fatally impaired. She was also unprotected against germs in the womb, leaving her susceptible to life-threatening infection.
Most babies are aborted after a rupture at such an early stage, but the baby's parents jumped at the chance after the hospital offered them what is normally high-risk prenatal surgery. "But here we were dealing with a healthy child and it was a question of significantly increasing its chances of survival," said Prof. Thomas Kohl, head of the German Center of Fetal Surgery and Minimally Invasive Therapy at Bonn University Clinic.
Surgeons inserted the operating device-no bigger than a ballpoint pen-into the fetal membranes through a small opening in the stomach of the baby's mother. Assisted by a camera and ultrasonic apparatus, they carefully moved this "fetoscope" via the mouth and into the trachea of the unborn baby. There a miniature latex balloon was inflated, blocking the respiratory channel so that the fluid continuously produced by the prenatal lung cannot drain away. This buildup of the fluid stimulated the growth of the baby's lung.
This was the first in which Professor Kohl also used albumin, which increases the amount of water collected in the lung and increases the effect of the balloon.
"Our little patient's lungs rose like yeast cake. The balloon stayed in the lungs for five days and during this period the volume of the lungs nearly doubled," said Professor Kohl.
The baby was born in the 33rd week of the pregnancy and is now a healthy one-year-old. The operation that saved her life was recently reported in Fetal Diagnosis and Therapy.
Humanoid teaches dentists to feel people's pain
TOKYO
Japan's future dentists may soon be able to better appreciate patients' pain by training on a humanoid robot that can mumble "ouch" when the drill hits a nerve. The robot, resembling an attractive young woman with long black hair and a pink sweater, can also listen to instructions and react to pain by moving her eyes or hands.
A group of robot and computer makers presented the high-tech dental patient in Tokyo at the recent 2007 International Robot Exhibition. The medical simulation robot, named "Simroid," is designed to be used for clinical training at dental schools, said Tatsuo Matsuzaki, an official at robot maker Kokoro Company Ltd., which developed the body and control system. The 5' 3" robot can say "it hurts" and frown when it feels uncomfortable from the dental drill.
"Because it's so real, dental trainees can see patients' feelings and will be able to develop good skills as they treat it, not as an object, but as a human being," Matsuzaki said. "The point is that we can share people's pain without hurting people."
Prof. Naotake Shibui of Nippon Medical School, which introduced the robot in September, said Simroid can help dentists learn how to communicate with patients. "Treatment technique is important but it's also important to feel what it's like to be a patient," he said.
But in case anyone thinks the robot is too real, it also has a sensor on the breast area that keeps track if it has been touched inappropriately, an engineer said.
Enzyme switch may open way to "eye in a dish"
PARIS
A key enzyme that triggers eye development has been identified, a discovery that could one day lead to "eye in a dish" replacement tissue for the visually impaired.
Writing in Nature, a team from the University of Warwick, central England, say the switch, called E-NTPDase2, is a so-called ectoenzyme, which is normally found on the outside surface of cells. They believe E-NTPDase2 initiates a molecular cascade that causes the eye to grow.
The researchers, experimenting on eight-cell frog embryos, introduced the enzyme into cells that would form the head area of the tadpole, and found that multiple eyes appeared to be created. When the enzyme was introduced to some cells that would form parts of the body, eye-like structures began to grow there, too, leading to tadpoles with an additional eye in their side, abdomen, or even along their tail.
The researchers believe that E-NTPDase2 latches onto an important signal- and energy-carrying molecule called adenosine triphosphate (ATP) and converts it into adenosine diphosphate (ADP).
Previous research has already identified the genes that initiate and direct eye development, but what has hitherto been unknown are the triggers-and the sequence of triggers-to turn them on. The Warwick team believe that a short burst of ATP, followed by a buildup of ADP, are the main signals for setting this genetic mechanism in motion.
E-NTPDase2 is known to play a role in human-eye development. Mutations in the gene, which lies on the ninth human chromosome, have been associated with severe head and eye defects.
"This new understanding of how eye development is triggered will greatly assist researchers exploring stem cells connected to eye development and opens up an avenue of research that could in just a few decades lead to the ability to produce an 'eye in a dish,'" the University of Warwich said.
Malaria's secrets unveiled
PARIS
Researchers in the United States believe they have gained an important insight as to why malaria causes only mild, flu-like symptoms in some individuals but in others causes coma and death. The explanation could lie in the molecular genetics of Plasmodium falciparum, the parasite that causes the disease, they report in Nature.
Aviv Regev of the Massachusetts Institute of Technology's Broad Institute and colleagues took blood from malaria-infected Senegalese children. They analyzed the proteins expressed by parasites in these samples and compared them with a well-known resource for lab study, the yeast Saccharomyces cervisiae.
The parasite, can be in one of three states as it circulates in the host's blood, the scientists said. One is that it actively grows, metabolizing carbohydrates as a source of energy; the second is a "starvation response" as it seeks other carbon sources for metabolism; and thirdly, a state of stress in the host environment.
"The results reveal a physiological diversity in the in vivo biology of the malaria parasite," they wrote, suggesting that this differing response could influence the severity of the disease and the response to drugs.
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