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Archive - Sep 19, 2011


Genetic Mutation Eliminates Fingerprints

Like DNA, fingerprints are unique to each person or set of identical twins. That makes them a valuable identification tool for everything from crime detection to international travel. But what happens when the tips of fingers are missing those distinctive patterns of ridges? It's not the premise for a science-fiction movie, but a real-life condition known as adermatoglyphia. It’s also known as "Immigration Delay Disease," because affected individuals experience difficulty in passing through security or checkpoints where fingerprint identification is required. Now Professor Eli Sprecher from Tel Aviv University's Sackler Faculty of Medicine and the Tel Aviv Sourasky Medical Center has identified the genetic mutation responsible for this unusual condition. The findings were published in the August 12, 2011 issue of the American Journal of Human Genetics. "Immigration Delay Disease" came to the attention of the medical community when it did just that — delay the attempts of one Swiss woman to cross the border into the United States, which requires that non-citizens be fingerprinted upon entry. Border control personnel were mystified when the woman informed them that she was unable to comply. Though an exceptionally rare condition — only four documented families are known to suffer from the disease worldwide — Professor Sprecher was inspired to delve deeper into the causes of the condition, which, in addition to causing an absence of fingerprints, also leads to a reduction in the number of sweat glands. Abnormal fingerprints can also be a warning sign of more severe disorders. Scientists know that fingerprints are fully formed 24 weeks after fertilization, and do not change throughout our lives.

Scientists Find Earliest Known Evidence of 1918 Influenza Pandemic

Examination of lung tissue and other autopsy material from 68 American soldiers who died of respiratory infections in 1918 has revealed that the influenza virus that eventually killed 50 million people worldwide was circulating in the United States at least four months before the 1918 influenza reached pandemic levels that fall. The study, using tissues preserved since 1918, was led by Dr. Jeffery K. Taubenberger of the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health. The study was published online on September 19, 2011, in PNAS. The researchers found proteins and genetic material from the 1918 influenza virus in specimens from 37 of the soldiers, including four who died between May and August 1918, months before the pandemic peaked. These four cases are the earliest 1918 pandemic influenza cases they know to be documented anywhere in the world, the scientists say. The clinical disease and tissue damage seen in the pre-pandemic cases were indistinguishable from those evident in cases that occurred during the height of the pandemic. This suggests, says Dr. Taubenberger, that over the course of the pandemic, the virus did not undergo a dramatic change that could explain the unusually high mortality it ultimately caused. In the current study, the autopsy materials showed that the virus replicated not only in the upper respiratory tract but also the lower respiratory tract, in a pattern very similar to that of the 2009 pandemic influenza virus. The team also found evidence that two virus variants were circulating in 1918. In one, a key viral protein called hemagglutinin bound well to receptors on human respiratory cells, while the hemagglutinin from the other variant bound less efficiently.